Search

LncRNA XIST and Nav1.7 have been identified to be significantly associated with the onset of osteoarthritis. Prim-O-glucosylcimifugin (POG) has antiinflammatory and analgesic effects in treating osteoarthritis (OA). However, its molecular mechanism of action remains unclear. This research investigated whether POG inhibits OA cartilage degeneration by regulating Nav1.7 through lncRNA XIST. We observed the relationship between lncRNA XIST and Nav1.7 through in vivo and in vitro experiments, and utilized lentiviral plasmids for XIST overexpression to further validate the protective effect of POG against OA. In vivo experiments revealed the close association of improving OA cartilage morphological changes by POG with lncRNA XIST and Nav1.7 downregulation and related proteins expression. In vitro experiments demonstrated significantly up-regulated lncRNA XIST and Nav1.7 expression in IL1β-induced chondrocytes, and their levels and related protein expression decreased after POG intervention. FISH indicated that POG attenuated the fluorescence intensity of lncRNA XIST in chondrocytes. RT-PCR and Western blot assays revealed the positive correlation of lncRNA XIST and Nav1.7 expression in chondrocytes. Additionally, flow cytometry results revealed that POG intervention reduced OA chondrocyte apoptosis. Therefore, we conclude that POG can mediate lncRNA XIST to regulate Nav1.7 to delay cartilage degeneration, which is an effective way to treat OA. However, lncRNA XIST is not the only target for regulation, and further discussion is needed., Competing Interests: Declaration of Competing Interest The authors declare that none of the work reported in this study could have been influenced by any known competing financial interests or personal relationships., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Oral cancers are a significant global health concern, with a high incidence of treatment failure primarily due to the development of drug resistance. Long non-coding RNAs (lncRNAs) have emerged as critical regulators of gene expression, playing pivotal roles in various cellular processes, including tumor progression and response to therapy. This review explores the multifaceted roles of lncRNAs in the development of drug resistance in oral cancers. We highlight the mechanisms by which lncRNAs modulate drug efflux, apoptosis, epithelial-mesenchymal transition (EMT), and other pathways associated with chemoresistance. Key lncRNAs implicated in resistance to commonly used chemotherapeutic agents in oral cancers are discussed, along with their potential as therapeutic targets. Understanding the involvement of lncRNAs in drug resistance mechanisms offers promising avenues for overcoming treatment barriers and improving patient outcomes. This review underscores the need for further research to elucidate the precise roles of lncRNAs in oral cancer resistance and their translation into clinical interventions., Competing Interests: Declaration of Competing Interest The authors declare no conflict of interest., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

The Polypyrimidine Tract-Binding Protein-Associated Splicing Factor (PSF), a component of the Drosophila Behavior/Human Splicing (DBHS) complex, plays a pivotal role in cancer pathogenesis. The epigenetic regulation mediated by PSF and long noncoding RNA (lncRNA), along with PSF's alternative splicing activity, has been implicated in promoting cancer cell proliferation, migration, invasion, metastasis, and drug resistance in various human cancers. Recent research highlights the therapeutic promise of targeting the PSF-lncRNA interaction to combat aggressive malignancies, making it a compelling target for cancer therapy. This review offers a detailed synthesis of the current understanding of PSF's role in oncogenic pathways and recent progress in identifying inhibitors of PSF-lncRNA interactions. Furthermore, it discusses the potential of using these inhibitors in cancer treatment strategies, especially as adjuncts to immune checkpoint blockade therapies to improve the efficacy of anti-PD-(L)1 treatments in Glioblastoma Multiforme (GBM). By outlining the interaction patterns of existing PSF-lncRNA inhibitors, this article aims to guide the development and refinement of future pharmacological interventions., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Peritoneal metastasis (PM) pathophysiology is complex and not fully understood. PM, originating from gastrointestinal (GI) cancer, is a condition that significantly worsens patient prognosis due to its complex nature and limited treatment options. The non-coding RNAs (ncRNAs) have been shown to play pivotal roles in cancer biology, influencing tumorigenesis, progression, metastasis, and therapeutic resistance. Increasing evidence has demonstrated the regulatory functions of different classes of ncRNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) in PM. Identifying biomarkers for early detection of PM is a crucial step towards improving patient outcomes, and how ncRNA profiles correlate with survival rates, response to therapy, and recurrence risks have raised much attention in recent years. Additionally, exploring innovative therapeutic approaches utilizing ncRNAs, such as targeted therapy and gene silencing, may offer new horizons in treating this dire condition. Recent advances in systemic treatments and the development of novel loco-regional therapies have opened doors to multimodal treatment approaches. Radical surgeries combined with hyperthermic intraperitoneal chemotherapy (HIPEC) have shown promising results, leading to extended patient survival. Current research is focused on the molecular characterization of PM, which is crucial for early detection and developing future therapeutic strategies. By summarizing the latest findings, this study underscores the transformative potential of ncRNAs in enhancing the diagnosis, prognosis, and treatment of PM in GI cancer, paving the way for more personalized and effective clinical strategies., Competing Interests: Declaration of Competing Interest The authors declare no conflict of interest., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

The gastrointestinal tract is chronically inflamed in ulcerative colitis (UC), which has a complicated etiology involving immunological, environmental, and genetic factors. The inflammatory response that is typical of UC is significantly regulated via the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway. Latest research has displayed that NF-κB signaling is controlled by three main types of non-coding RNAs (ncRNAs): circular RNAs (circRNAs), long non-coding RNAs (lncRNAs), and microRNAs (miRNAs). These ncRNAs can change the expression of key genes within the NF-κB pathway by acting as molecular sponges, transcriptional regulators, and epigenetic modifiers. This review synthesizes current knowledge on the functions by which ncRNAs modulate NF-κB signaling in UC, discusses their potential as biomarkers for disease prognosis and diagnosis, and explores their therapeutic potential. Understanding the intricate interactions between ncRNAs and NF-κB signaling may provide novel insights into UC pathogenesis and targeted therapeutic strategies., Competing Interests: Declaration of Competing Interest The authors declare no competing interests, (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

In the last decade, researchers have paid much attention to the role of noncoding RNA molecules in human diseases. Among the most important of these molecules are LncRNAs, which are RNA molecules with a length of more than 200 nucleotides. LncRNAs can regulate gene expression through various mechanisms, such as binding to DNA sequences and interacting with miRNAs. Studies have shown that LncRNAs may be valuable therapeutic targets in treating various cancers, including upper-gastrointestinal cancers. Upper gastrointestinal cancers, mainly referring to esophageal and gastric cancers, are among the deadliest gastrointestinal cancers. Despite notable advances, traditional chemotherapy remains a common strategy for treating these cancers. However, chemoresistance poses a significant obstacle to the effective treatment of upper gastrointestinal cancers, resulting in a low survival rate. Chemoresistance arises from various events, such as the enhancement of efflux and detoxification of chemotherapy agents, reduction of drug uptake, alteration of drug targeting, reduction of prodrug activation, strengthening of EMT and stemness, and the attenuation of apoptosis in cancerous cells. Tumor microenvironment also plays an important role in chemoresistance. Interestingly, a series of studies have revealed that LncRNAs can influence important mechanisms associated with some of the aforementioned events and may serve as promising targets for mitigating chemoresistance in upper gastrointestinal cancers. In this review paper, following a concise overview of chemoresistance mechanisms in upper gastrointestinal cancers, we will review the most intriguing findings of these investigations in detail., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Aims: To investigate the molecular mechanism of osteoclast-derived exosomes in osteoporosis., Main Methods: RANKL induced osteoclast model was screened for significantly differentially expressed lncRNAs and mRNAs by whole RNA sequencing. Exosomes were characterized using electron microscopy, western blotting and nanosight. Overexpression or knockdown of AW011738 was performed to explore its function. The degree of osteoporosis in an osteoporosis model was assessed by mirco-CT. The osteoclast model, osteoblast differentiation ability and the molecular mechanism of lncRNA AW011738/miR-24-2-5p/TREM1 axis in osteoporosis were assessed by dual luciferase reporter gene assay, Western blotting (WB), immunofluorescence and ALP staining. Bioinformatics was used to predict interactions of key osteoporosis-related genes with miRNAs, transcription factors, and potential drugs after upregulation of AW011738. To predict the protein-protein interaction (PPI) network associated with key genes, GO and KEGG analyses were performed on the key genes. The ssGSVA was used to predict changes in the immune microenvironment., Key Findings: Osteoclast-derived exosomes containing lncRNA AW011738 decreased the osteogenesis-related markers and accelerated bone loss in OVX mice. Osteoclast (si-AW011738)-derived exosomes showed a significant increase in biomarkers of osteoblast differentiation in vitro compared to the si-NC group. As analyzed by mirco-CT, tail vein injected si-AW011738 OVX mice were less osteoporotic than the control group. AW011738 inhibited osteoblast differentiation by regulating TREM1 expression through microRNA. Meanwhile, overexpression of miR-24-2-5p inhibited TREM1 expression to promote osteoblast differentiation., Significance: Osteoclast-derived exosomes containing lncRNA AW011738 inhibit osteogenesis in MC3T3-E1 cells through the lncRNA AW011738/miR-24-2-5p/TREM1 axis and exacerbate osteoporosis in OVX mice., Competing Interests: Declaration of Competing Interest The authors attest that they do not have any competing interests to report., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Osteoporosis, characterized by compromised bone density and microarchitecture, represents a significant global health challenge, particularly in aging populations. This comprehensive review delves into the intricate signaling pathways implicated in the pathogenesis of osteoporosis, providing valuable insights into the pivotal role of signal transduction in maintaining bone homeostasis. The exploration encompasses cellular signaling pathways such as Wnt, Notch, JAK/STAT, NF-κB, and TGF-β, all of which play crucial roles in bone remodeling. The dysregulation of these pathways is a contributing factor to osteoporosis, necessitating a profound understanding of their complexities to unveil the molecular mechanisms underlying bone loss. The review highlights the pathological significance of disrupted signaling in osteoporosis, emphasizing how these deviations impact the functionality of osteoblasts and osteoclasts, ultimately resulting in heightened bone resorption and compromised bone formation. A nuanced analysis of the intricate crosstalk between these pathways is provided to underscore their relevance in the pathophysiology of osteoporosis. Furthermore, the study addresses some of the most crucial long non-coding RNAs (lncRNAs) associated with osteoporosis, adding an additional layer of academic depth to the exploration of immune system involvement in various types of osteoporosis. Finally, we propose that SKP1 can serve as a potential biomarker in osteoporosis., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Inflammatory bowel disease (IBD) is a chronic relapsing disease of the gastrointestinal (GI) system that includes two groups, Crohn's disease (CD) and ulcerative colitis (UC). To cope with these two classes of IBD, the investigation of pathogenic mechanisms and the discovery of new diagnostic and therapeutic approaches are crucial. Long non-coding RNAs (lncRNAs) which are non-coding RNAs with a length of longer than 200 nucleotides have indicated significant association with the pathology of IBD and strong potential to be used as accurate biomarkers in diagnosing and predicting responses to the IBD treatment. In the current review, we aim to investigate the role of lncRNAs in the pathology and development of IBD. We first describe recent advances in research on dysregulated lncRNAs in the pathogenesis of IBD from the perspective of epithelial barrier function, intestinal immunity, mitochondrial function, and intestinal autophagy. Then, we highlight the possible translational role of lncRNAs as therapeutic targets, diagnostic biomarkers, and predictors of therapeutic response in colon tissues and plasma samples. Finally, we discuss the potential of extracellular vesicles and their lncRNA cargo in the pathophysiology, diagnosis, and treatment of IBD., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Noncoding RNAs (ncRNAs) do not participate in protein-coding. Ferroptosis is a newly discovered form of cell death mediated by reactive oxygen species and lipid peroxidation. Recent studies have shown that ncRNAs such as microRNAs, long noncoding RNAs, circular RNAs, and ferroptosis are involved in the occurrence and development of osteosarcoma (OS). Studies have confirmed that ncRNAs participate in the development of OS by regulating the ferroptosis. However, systematic summary on this topic are still lacking. This review summarises the potential role of ncRNAs in the diagnosis, treatment, drug resistance, and prognosis of OS and the basis for diagnosing, preventing, and treating clinical OS and developing effective drugs. This review summarises the latest research progress on ncRNAs that regulate ferroptosis in OS, attempts to clarify the molecular mechanisms by which ncRNAs regulate ferroptosis in the pathogenesis of OS, and elaborates on the involvement of ferroptosis in OS from the perspective of ncRNAs., Competing Interests: Declaration of Competing Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Metabolic reprogramming plays critical roles in the development and progression of tumor by providing cancer cells with a sufficient supply of nutrients and other factors needed for fast-proliferating. Emerging evidence indicates that long noncoding RNAs (lncRNAs) are involved in the initiation of metastasis via regulating the metabolic reprogramming in various cancers. In this paper, we aim to summarize that lncRNAs could participate in intracellular nutrient metabolism including glucose, amino acid, lipid, and nucleotide, regardless of whether lncRNAs have tumor-promoting or tumor-suppressor function. Meanwhile, modulation of lncRNAs in glucose metabolic enzymes in glycolysis, pentose phosphate pathway and tricarboxylic acid cycle (TCA) in cancer is reviewed. We also discuss therapeutic strategies targeted at interfering with enzyme activity to decrease the utilization of glucoses, amino acid, nucleotide acid and lipid in tumor cells. This review focuses on our current understanding of lncRNAs participating in cancer cell metabolic reprogramming, paving the way for further investigation into the combination of such approaches with existing anti-cancer therapies., Competing Interests: Declaration of Competing Interest There are no conflicts of interest to report., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

The intricate crosstalk between long noncoding RNAs (lncRNAs) and epigenetic modifications such as chromatin/histone methylation and acetylation offer new perspectives on the pathogenesis and treatment of kidney diseases. lncRNAs, a class of transcripts longer than 200 nucleotides with no protein-coding potential, are now recognized as key regulatory molecules influencing gene expression through diverse mechanisms. They modulate the epigenetic modifications by recruiting or blocking enzymes responsible for adding or removing methyl or acetyl groups, such as DNA, N6-methyladenosine (m6A) and histone methylation and acetylation, subsequently altering chromatin structure and accessibility. In kidney diseases such as acute kidney injury (AKI), chronic kidney disease (CKD), diabetic nephropathy (DN), glomerulonephritis (GN), and renal cell carcinoma (RCC), aberrant patterns of DNA/RNA/histone methylation and acetylation have been associated with disease onset and progression, revealing a complex interplay with lncRNA dynamics. Recent studies have highlighted how lncRNAs can impact renal pathology by affecting the expression and function of key genes involved in cell cycle control, fibrosis, and inflammatory responses. This review will separately address the roles of lncRNAs and epigenetic modifications in renal diseases, with a particular emphasis on elucidating the bidirectional regulatory effects and underlying mechanisms of lncRNAs in conjunction with DNA/RNA/histone methylation and acetylation, in addition to the potential exacerbating or renoprotective effects in renal pathologies. Understanding the reciprocal relationships between lncRNAs and epigenetic modifications will not only shed light on the molecular underpinnings of renal pathologies but also present new avenues for therapeutic interventions and biomarker development, advancing precision medicine in nephrology., Competing Interests: Declaration of Competing Interest The authors have declared that no competing interest exists., (Copyright © 2024. Published by Elsevier Masson SAS.)

Long non-coding RNAs (lncRNAs) are pivotal controllers of gene expression through epigenetic mechanisms, Methylation, a prominent area of study in epigenetics, significantly impacts cellular processes. Various RNA base methylations, including m6A, m5C, m1A, and 2'-O-methylation, profoundly influence lncRNA folding, interactions, and stability, thereby shaping their functionality. LncRNAs and methylation significantly contribute to tumor development, especially in lung cancer. Their roles encompass cell differentiation, proliferation, the generation of cancer stem cells, and modulation of immune responses. Recent studies have suggested that dysregulation of lncRNA methylation can contribute to lung cancer development. Furthermore, methylation modifications of lncRNAs hold potential for clinical application in lung cancer. Dysregulated lncRNA methylation can promote lung cancer progression and may offer insights into potential biomarker or therapeutic target. This review summarizes the current knowledge of lncRNA methylation in lung cancer and its implications for RNA epigenetics and pulmonary diseases., Competing Interests: Declaration of Competing Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Purpose: Renal interstitial fibrosis is a pathological manifestation of the progression of diabetic kidney disease (DKD). Dendrobium officinale polysaccharides (DOP), one of the major active components of Dendrobium officinale, have hypoglycemic and hypolipidemic effects and are used clinically to treat diabetes. However, the role of DOP in delaying DKD progression remains unclear. This study aimed to explore the potential mechanisms by which DOP delays DKD renal interstitial fibrosis., Methods: Using db/db mice as a model of DKD, we administered DOP by gavage and observed its therapeutic effectiveness. Employing ASO technology, we knocked down lncRNA XIST expression in kidney tissues and detected the expression of lncRNA XIST, TGF-β1, and renal interstitial fibrosis-related molecules., Results: DOP was primarily composed of monosaccharides, with 91.57% glucose and 1.41% mannose, forming a spheroid-like structure. It has a high polydispersity index with an Mw/Mn of 6.146, and the polysaccharides are mainly connected by 4-Man(p) and 4-Glc(p) linkages. In the kidneys of db/db mice, lncRNA XIST and TGF-β1 are highly expressed; however, their expression is significantly reduced after gastric infusion with DOP, and upon knockdown of lncRNA XIST, it might delay the progression of renal interstitial fibrosis in DKD., Conclusion: DOP may delay the progression of DKD renal interstitial fibrosis through the regulation of the LncRNA XIST/TGF-β1 related fibrotic pathway. This provides a new perspective for clinical strategies to delay the progression of DKD renal interstitial fibrosis., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

An increasing number of studies have shown that FAM83A, a member of the family with sequence similarity 83 (FAM83), which consists of eight members, is a key tumor therapeutic target involved in multiple signaling pathways. It has been reported that FAM83A plays essential roles in the regulation of Wnt/β-catenin, EGFR, MAPK, EMT, and other signaling pathways and physiological processes in models of pancreatic cancer, lung cancer, breast cancer, and other malignant tumors. Moreover, the expression of FAM83A could be significantly affected by multiple noncoding RNAs that are dysregulated in malignant tumors, the dysregulation of which is essential for the malignant process. Among these noncoding RNAs, the most noteworthy is the antisense long noncoding (Lnc) RNA of FAM83A itself (FAM83A-AS1), indicating an outstanding synergistic carcinogenic effect between FAM83A and FAM83A-AS1. In the present study, the specific mechanisms by which FAM83A and FAM83A-AS1 cofunction in the Wnt/β-catenin and EGFR signaling pathways were reviewed in detail, which will guide subsequent research. We also described the applications of FAM83A and FAM83A-AS1 in tumor therapy and provided a certain theoretical basis for subsequent drug target development and combination therapy strategies., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Masson SAS.)

Myocardial infarction (MI) is the leading cause of heart failure (HF), accounting for high mortality and morbidity worldwide. As a consequence of ischemia/reperfusion injury during MI, multiple cellular processes such as oxidative stress-induced damage, cardiomyocyte death, and inflammatory responses occur. In the next stage, the proliferation and activation of cardiac fibroblasts results in myocardial fibrosis and HF progression. Therefore, developing a novel therapeutic strategy is urgently warranted to restrict the progression of pathological cardiac remodeling. Recently, targeting long non-coding RNAs (lncRNAs) provided a novel insight into treating several disorders. In this regard, numerous investigations have indicated that several lncRNAs could participate in the pathogenesis of MI-induced cardiac remodeling, suggesting their potential therapeutic applications. In this review, we summarized lncRNAs displayed in the pathophysiology of cardiac remodeling after MI, emphasizing molecular mechanisms. Also, we highlighted the possible translational role of lncRNAs as therapeutic targets for this condition and discussed the potential role of exosomes in delivering the lncRNAs involved in post-MI cardiac remodeling., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

The pivotal regulatory role of non-coding RNAs (ncRNAs), especially exosomal ncRNAs, in ferroptosis significantly influences cancer cell fate. This review explores their involvement across various human cancers, focusing on microRNAs (miRNA), long non-coding RNAs (lncRNA), and circular RNAs (circRNA). These ncRNAs either stimulate or inhibit ferroptosis by targeting key components, impacting cancer susceptibility to this form of cell death. Specific studies in lung, gastric, liver, cervical, bladder, pancreatic, and osteosarcoma cancers underscore the crucial role of exosomal ncRNAs in modulating ferroptosis, influencing cancer progression, and therapeutic responses. Emphasizing the therapeutic potential of exosomal ncRNAs, we discuss their ability to deliver circRNA, miRNA, and lncRNA to target cells. Despite being in early stages with challenges in bioengineering for drug delivery, these studies hold promise for future clinical applications. Noteworthy findings include inhibiting exosome production to overcome ferroptosis resistance in lung adenocarcinoma and the potential of exosomal DACT3-AS1 to sensitize gastric cancer cells to ferroptosis. The review concludes by highlighting exosomal ncRNAs like miR-4443 and miR-660-5p as promising therapeutic targets, offering avenues for precise cancer interventions by modulating signaling pathways and sensitizing cells to ferroptosis. Overall, this review enhances our understanding of cancer pathogenesis and presents new horizons for targeted therapeutic interventions, revealing the intricate interplay between exosomal ncRNAs and ferroptosis., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Masson SAS.)

Viral infections present significant challenges to human health, underscoring the importance of understanding the immune response for effective therapeutic strategies. Immune cell activation leads to dynamic changes in gene expression. Numerous studies have demonstrated the crucial role of long noncoding RNAs (lncRNAs) in immune activation and disease processes, including viral infections. This review provides a comprehensive overview of lncRNAs expressed in immune cells, including CD8 T cells, CD4 T cells, B cells, monocytes, macrophages, dendritic cells, and granulocytes, during both acute and chronic viral infections. LncRNA-mediated gene regulation encompasses various mechanisms, including the modulation of viral replication, the establishment of latency, activation of interferon pathways and other critical signaling pathways, regulation of immune exhaustion and aging, and control of cytokine and chemokine production, as well as the modulation of interferon-stimulated genes. By highlighting specific lncRNAs in different immune cell types, this review enhances our understanding of immune responses to viral infections from a lncRNA perspective and suggests potential avenues for exploring lncRNAs as therapeutic targets against viral diseases., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Long non-coding RNAs (lncRNAs) are a type of RNAs that are more than 200 nucleotides without protein-coding potential. In recent years, more and more attention has been paid to the role of lncRNAs in cancer pathogenesis. LncRNA KCNQ1 overlapping transcript 1 (KCNQ1OT1) is located on chromosome 11p15.5 with a total length of 91 kb and is highly expressed in various malignancies, which is closely related to tumor growth, lymph node metastasis, survival cycle and recurrence rate. In addition, KCNQ1OT1 is involved in the regulation of PI3K/AKT and Wnt/β-catenin signaling pathways. In this review, the mechanism and related progress of KCNQ1OT1 in different cancers were reviewed. It was found that KCNQ1OT1 can stabilize mRNA expression through sponging miRNA, which not only induced tumor cell proliferation, migration, invasion, drug resistance, epithelial-mesenchymal transition (EMT) and inhibited cell apoptosis in vitro, but also promoted tumor growth and metastasis in vivo. Therefore, as a new biomarker and therapeutic target, KCNQ1OT1 has broad prospects for the diagnosis and treatment of different cancers., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

In recent years, research on the mechanism of bone destruction in rheumatoid arthritis (RA) has remained in the initial stages, and the mechanism has not been fully elucidated to date. Recent studies have shown that long noncoding RNAs (lncRNAs) participate in RA bone destruction via autophagy, but the specific regulatory mechanism of lncRNA-mediated autophagy is unclear. Therefore, in this article, we review the mechanisms of lncRNA-mediated autophagy in fibroblast-like synoviocytes and chondrocytes in RA bone destruction. We explain that lncRNAs mediate autophagy and participate in many specific pathological processes of RA bone destruction by regulating signalling pathways and the expression of target genes. Specific lncRNAs can be used as markers for molecular diagnosis, mechanistic regulation, treatment and prognosis of RA., Competing Interests: Declaration of Competing Interest All the authors’ names are arranged according to their contributions to the article, and they have read through the full text and approved the submission of the final version. Their signatures on the article are undisputed. All the author have no conflict of interest to declare., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Osteoarthritis (OA) is an extremely common type of chronic progressive disease in clinical practice. lncRNA TUC339 has a close association with bone marrow mesenchymal stem cell (BMSC) and an important impact on organismal inflammation. However, the mechanism of BMSC-derived lncRNA TUC339 on OA was poorly understood. In this study, we found that TUC339 was lower in the research group than in the control group and it was negatively correlated with IL-6, IL-8 and TNF-α. Prognosis TUC339 was lower in patients with recurrent OA than in those without recurrence, and ROC analysis manifested that TUC339 had a better predictive value for recurrence of OA. Phenotypic identification revealed elevated expression of CD29 and CD44 in BMSCs and TSG101, CD63 and CD81 in BMSCs-exosome (BMSCs-exo), with a stem cell versus exosome phenotype. Finally, animal experiments improved significantly in joint injury in the BMSCs-exo and TUC339-overexpression vector groups compared with control groups. Similarly, the activity of chondrocytes was enhanced, and apoptosis was reduced in the BMSCs-exo group versus the TUC339-overexpression vector group of rats. Study demonstrated that BMSCs-exo improves OA by elevating the expression of TUC339 to promote M1-type mø to M2-type polarization, suppressing inflammation and promoting chondrocyte activity, which provides a reliable basis for future transplantation therapy of MSCs for OA., Competing Interests: Declaration of Competing Interest The authors have no relevant financial or non-financial interests to disclose., (Copyright © 2023. Published by Elsevier Masson SAS.)

Periodontitis is an inflammatory disease characterized by the pathological loss of alveolar bone and the adjacent periodontal ligament. It is considered a disease that imposes a substantial health burden, with an incidence rate of 20-50%. The etiology of periodontitis is multifactorial, with genetic factors accounting for approximately half of severe cases. Studies have revealed that long non-coding RNAs (lncRNAs) play a pivotal role in periodontitis pathogenesis. Accumulating evidence suggests that lncRNAs have distinct regulatory mechanisms, enabling them to control numerous vital processes in periodontal cells, including osteogenic differentiation, inflammation, proliferation, apoptosis, and autophagy. In this review, we summarize the diverse roles of lncRNAs in the pathogenesis of periodontitis, shedding light on the underlying mechanisms of disease development. By highlighting the potential of lncRNAs as biomarkers and therapeutic targets, this review offers a new perspective on the diagnosis and treatment of periodontitis, paving the way for further investigation into the field of lncRNA-based therapeutics., Competing Interests: Declaration of Competing Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Tumor metastasis is the main reason for cancer-related death, but there is still a lack of effective therapeutic to inhibit tumor metastasis. Therefore, the discovery and study of new tumor metastasis regulators is a prominent measure for cancer diagnosis and treatment. Long non-coding RNA (lncRNA) is a type of non-coding RNAs over 200 bp in length. It has been shown that the abnormally expressed lncRNAs promote tumor metastasis by participating in the epithelial-to-mesenchymal transition (EMT) process, altering the metastatic tumor microenvironment, or changing the extracellular matrix. It is,thus, critical to explore the regulation of lncRNAs expression in cells and the molecular mechanism of lncRNA-mediated cancer metastasis. Simultaneously, it has been shown that lncRNA is one kind of the main components of exosomes, which protects lncRNAs from being rapidly degraded. Meanwhile, the components of exosomes are parent-specific, making exosomal lncRNAs to be potential tumor metastasis markers and therapeutic targets. In view of this, we also summarized the aberrant enrichment of lncRNAs in exosomes and their role in metastatic cancer. The aberrant lncRNAs and exosomal lncRNAs gradually become biomarkers and therapeutic targets for tumor metastatic, and the potential of lncRNAs in therapeutics are studied here. Besides, the lncRNA-related databases, which could greatly facilitate in the study of lncRNAs and exosomal lncRNAs in metastatic of cancer are included in this review., Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interest and consent for publication., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Septic acute kidney injury (SAKI) is one of the most common and life-threatening complications of sepsis. Patients with SAKI have increased mortality. However, the underlying pathogenesis is unclear, and the treatment targeting SAKI is unsatisfactory. Thus, identifying optimal biomarkers for SAKI diagnosis and treatment is an urgent requisite. Accumulating evidence indicates that noncoding RNAs (ncRNAs) are involved in the occurrence and progression of SAKI. In the present review, we summarized the studies of ncRNAs in SAKI, including microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs). The ncRNAs are divided into protective and damage factors according to their role in SAKI, and their expression patterns, functions, and molecular mechanisms were elaborated. Next, we proposed that ncRNAs have the potential to be diagnostic and prognostic biomarkers for SAKI and as new therapeutic targets. This review aimed to provide a comprehensive overview of ncRNAs in SKAI and explored the clinical value of ncRNAs as ideal biomarkers of SAKI., Competing Interests: Declaration of Competing Interest The authors declare no conflict of interest., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Bladder cancer (BC) is a common and serious type of cancer that ranks among the top ten most prevalent malignancies worldwide. Due to the high occurrence rate of BC, the aggressive nature of cancer cells, and their resistance to medication, managing this disease has become a growing challenge in clinical care. Long noncoding RNAs (lncRNAs) are a group of RNA transcripts that do not code for proteins and are more than 200 nucleotides in length. They play a significant role in controlling cellular pathways and molecular interactions during the onset, development and progression of different types of cancers. Recent advancements in high-throughput gene sequencing technology have led to the identification of various differentially expressed lncRNAs in BC, which indicate abnormal expression. In this review, we summarize that these lncRNAs have been found to impact several functions related to the development of BC, including proliferation, cell growth, migration, metastasis, apoptosis, epithelial-mesenchymal transition, and chemo- and radio-resistance. Additionally, lncRNAs may improve prognosis prediction for BC patients, indicating a future use for them as prognostic and diagnostic biomarkers for BC patients. This review highlights that genetic tools and anti-tumor agents, such as CRISPR/Cas systems, siRNA, shRNA, antisense oligonucleotides, and vectors, have been created for use in preclinical cancer models. This has led to a growing interest in using lncRNAs based on positive research findings., Competing Interests: Declaration of Competing Interest Please declare any financial or personal interests that might be potentially viewed to influence the work presented. Interests could include consultancies, honoraria, patent ownership or other. If there are none state ‘there are none’., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Brain tumors, which are highly malignant, pose a significant threat to health and often result in substantial rates of mortality and morbidity worldwide. The brain cancer therapy has been challenging due to obstacles such as the BBB, which hinders effective delivery of therapeutic agents. Additionally, the emergence of drug resistance further complicates the management of brain tumors. TMZ is utilized in brain cancer removal, but resistance is a drawback. ncRNAs are implicated in various diseases, and their involvement in the cancer is particularly noteworthy. The focus of the current manuscript is to explore the involvement of ncRNAs in controlling drug resistance, specifically in the context of resistance to the chemotherapy drug TMZ. The review emphasizes the function of ncRNAs, particularly miRNAs, in modulating the growth and invasion of brain tumors, which significantly influences their response to TMZ treatment. Through their interactions with various molecular pathways, miRNAs are modulators of TMZ response. Similarly, lncRNAs also associate with molecular pathways and miRNAs, affecting the efficacy of TMZ chemotherapy. Given their functional properties, lncRNAs can either induce or suppress TMZ resistance in brain tumors. Furthermore, circRNAs, which are cancer controllers, regulate miRNAs by acting as sponges, thereby impacting the response to TMZ chemotherapy. The review explores the correlation between ncRNAs and TMZ chemotherapy, shedding light on the underlying molecular pathways involved in this process., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Noncoding ribonucleic acids (ncRNAs) are a class of ribonucleic acids (RNAs) that carry cellular information and perform essential functions. This class encompasses various RNAs, such as small nuclear ribonucleic acids (snRNA), small interfering ribonucleic acids (siRNA) and many other kinds of RNA. Of these, circular ribonucleic acids (circRNAs) and long noncoding ribonucleic acids (lncRNAs) are two types of ncRNAs that regulate crucial physiological and pathological processes, including binding, in several organs through interactions with other RNAs or proteins. Recent studies indicate that these RNAs interact with various proteins, including protein 53, nuclear factor-kappa B, vascular endothelial growth factor, and fused in sarcoma/translocated in liposarcoma, to regulate both the histological and electrophysiological aspects of cardiac development as well as cardiovascular pathogenesis, ultimately leading to a variety of genetic heart diseases, coronary heart disease, myocardial infarction, rheumatic heart disease and cardiomyopathies. This paper presents a thorough review of recent studies on circRNA and lncRNAprotein binding within cardiac and vascular cells. It offers insight into the molecular mechanisms involved and emphasizes potential implications for treating cardiovascular diseases., Competing Interests: Declaration of Competing Interest The manuscript has not been published before and is not being considered for publication elsewhere. We declare there is no conflict of interest., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Cardiovascular disease (CVD) is a major contributor to increasing morbidity and mortality worldwide and seriously threatens human health and life. Cardiomyocyte death is considered the pathological basis of various CVDs, including myocardial infarction, heart failure, and aortic dissection. Multiple mechanisms, such as ferroptosis, necrosis, and apoptosis, contribute to cardiomyocyte death. Among them, ferroptosis is an iron-dependent form of programmed cell death that plays a vital role in various physiological and pathological processes, from development and aging to immunity and CVD. The dysregulation of ferroptosis has been shown to be closely associated with CVD progression, yet its underlying mechanisms are still not fully understood. In recent years, a growing amount of evidence suggests that non-coding RNAs (ncRNAs), particularly microRNAs, long non-coding RNAs, and circular RNAs, are involved in the regulation of ferroptosis, thus affecting CVD progression. Some ncRNAs also exhibit potential value as biomarker and/or therapeutic target for patients with CVD. In this review, we systematically summarize recent findings on the underlying mechanisms of ncRNAs involved in ferroptosis regulation and their role in CVD progression. We also focus on their clinical applications as diagnostic and prognostic biomarkers as well as therapeutic targets in CVD treatment. DATA AVAILABILITY: No new data were created or analyzed in this study. Data sharing is not applicable to this article., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Rheumatoid Arthritis (RA) is a chronic autoimmune disease. Its main feature is inflammation of synovial tissue with irreversible joint damage and severe physical damage. Non-coding RNAs (ncRNAs) are a class of RNAs that do not have the ability to encode proteins but are vital regulators that mediate many fundamental cellular processes and play an essential role in the pathogenesis of RA. Multiple verified ncRNAs have been confirmed as a prospective biomarkers for diagnosing and treating RA. In this paper, we aim to sort out the role of ncRNAs in the pathogenesis of RA and provide new ideas for the diagnosis and treatment of RA., Competing Interests: Declaration of Competing Interest All financial, commercial or other relationships that might be perceived by the academic community as representing a potential conflict of interest must be disclosed. If no such relationship exists, authors will be asked to confirm the following statement: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Long non-coding RNAs (lncRNAs) are commonly known for their important characters in cancer progression. LncRNA MAFG-antisense 1 (AS1) (MAFG-AS1) has been discovered as a novel oncogenic lncRNA for several years. Accumulating data have demonstrated abnormal overexpression of MAFG-AS1 in various human cancers, including breast, bladder, liver, gastric, and lung. Importantly, through regulating various microRNAs and cell signaling pathways, MAFG-AS1 has been demonstrated to exhibit various biological effects, including proliferation, metastasis, and epithelial-mesenchymal transition (EMT). Meanwhile, abnormal overexpression of MAFG-AS1 is closely linked with histological grade, TNM stage, extensive depth of invasion, poor OS, and lymph node metastasis (LNM). In the present review, the authors summarized the previous studies on the biological properties, molecular mechanisms, and clinicopathological characters of MAFG-AS1 in human cancers. In summary, MAFG-AS1 is a promising prognostic biological marker and potential therapeutic target for cancer treatment., Competing Interests: Declaration of Competing Interest The authors declare that there is no conflict of interest., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

The frequent metastasis of gastric cancer (GC) complicates the cure and therefore the development of effective diagnostic and therapeutic approaches is urgently necessary. In recent years, lncRNA has emerged as a drug target in the treatment of GC, particularly in the areas of cancer immunity, cancer metabolism, and cancer metastasis. This has led to the demonstration of the importance of these RNAs as prognostic, diagnostic and therapeutic agents. In this review, we provide an overview of the biological activities of lncRNAs in GC development and update the latest pathological activities, prognostic and diagnostic strategies, and therapeutic options for GC-related lncRNAs., Competing Interests: Conflict of Interest Statement This paper has been read and approved by all the authors and all of them declared no conflicts of interest., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Acute myeloid leukemia (AML) is a hematologic carcinoma that has seen a considerable improvement in patient prognosis because of genetic diagnostics and molecularly-targeted therapies. Nevertheless, recurrence and drug resistance remain significant obstacles to leukemia treatment. It is critical to investigate the underlying molecular mechanisms and find solutions. Non-coding RNAs (ncRNAs), such as microRNAs (miRNAs), circular RNAs, long non-coding RNAs, and pseudogenes, have been found to be crucial components in driving cancer. The competing endogenous RNA (ceRNA) mechanism has expanded the complexity of miRNA-mediated gene regulation. A great deal of literature has shown that ncRNAs are essential to the biological functions of the ceRNA network (ceRNET). NcRNAs can compete for the same miRNA response elements to influence miRNA-target RNA interactions. Recent evidence suggests that ceRNA might be a potential biomarker and therapeutic strategy. So far, however, there have been no comprehensive studies on ceRNET about AML. What is not yet clear is the clinical application of ceRNA in AML. This study attempts to summarize the development of research on the related ceRNAs in AML and the roles of ncRNAs in ceRNET. We also briefly describe the mechanisms of ceRNA and ceRNET. What's more significant is that we explore the clinical value of ceRNAs to provide accurate diagnostic and prognostic biomarkers as well as therapeutic targets. Finally, limitations and prospects are considered., Competing Interests: Declaration of Competing Interest The authors declare that there is no conflict of interest., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

With the rapid development of next-generation sequencing technology, several studies have shown that ncRNAs can act as competitive endogenous RNAs (ceRNAs) and are involved in various biological processes, such as proliferation, differentiation, apoptosis, and migration of breast cancer (BC) cells, and plays an important role in BC progression as a molecular target for its diagnosis, treatment, prognosis, and differentiation of subtypes and age groups of BC patients. Based on the description of ceRNA-related biological functions, this study screened and sorted the sequencing analysis and experimental verification conclusions of BC-related ceRNAs and found that the ncRNAs mediated ceRNA networks can promote the development of BC by promoting the expression of genes related to BC proliferation, drug resistance, and apoptosis, inducing the production of epithelial-mesenchymal transition (EMT) to promote metastasis and activating cancer-related signaling pathways., Competing Interests: Declaration of Competing Interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Neurological disorders with various etiologies impacting the nervous system are prevalent in clinical practice. Long non-coding RNA (lncRNA) molecules are functional RNA molecules exceeding 200 nucleotides in length that do not encode proteins, but participate in essential activities. Research indicates that lncRNAs may contribute to the pathogenesis of neurological disorders, and may be potential targets for their treatment. Phytochemicals in traditional Chinese herbal medicine (CHM) have been found to exert neuroprotective effects by targeting lncRNAs and regulating gene expression and various signaling pathways. We aim to establish the development status and neuroprotective mechanism of phytochemicals that target lncRNAs through a thorough literature review. A total of 369 articles were retrieved through manual and electronic searches of PubMed, Web of Science, Scopus and CNKI databases from inception to September 2022. The search utilized combinations of natural products, lncRNAs, neurological disorders, and neuroprotective effects as keywords. The included studies, a total of 31 preclinical trials, were critically reviewed to present the current situation and the progress in phytochemical-targeted lncRNAs in neuroprotection. Phytochemicals have demonstrated neuroprotective effects in preclinical studies of various neurological disorders by regulating lncRNAs. These disorders include arteriosclerotic ischemia-reperfusion injury, ischemic/hemorrhagic stroke, Alzheimer's disease, Parkinson's disease, glioma, peripheral nerve injury, post-stroke depression, and depression. Several phytochemicals exert neuroprotective roles through mechanisms such as anti-inflammatory, antioxidant, anti-apoptosis, autophagy regulation, and antagonism of Aβ-induced neurotoxicity. Some phytochemicals targeted lncRNAs and served a neuroprotective role by regulating microRNA and mRNA expression. The emergence of lncRNAs as pathological regulators provides a novel direction for the study of phytochemicals in CHM. Elucidating the mechanism of phytochemicals regulating lncRNAs will help to identify new therapeutic targets and promote their application in precision medicine., Competing Interests: Declaration of Competing Interest The authors wish to confirm that no significant financial support for this work influenced its outcome, and there are no known conflicts of interest associated with this publication., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

In recent years, breakthroughs in bioinformatics have been made with the discovery of many functionally significant non-coding RNAs (ncRNAs). The discovery of these ncRNAs has further demonstrated the multi-level characteristics of intracellular gene expression regulation, which plays an important role in assisting diagnosis, guiding clinical drug use and determining prognosis in the treatment process of various diseases. microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) are the three major types of ncRNAs that interact with each other. Studies have shown that lncRNAs and circRNAs can sponge miRNAs, thereby influencing normal physiological processes and regulating mRNA expression and, thus, the physiological state of cells. This paper summarizes the mechanism of action and research progress of the three ncRNA and seven types of modalities. This summary is intended to provide new ideas for diagnosing and treating diseases and researching and developing new drugs., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Glioblastoma multiforme (GBM) is one of the most common primary malignant brain tumors in adults. Due to the poor prognosis of patients, the median survival time of GBM is often less than 1 year. Therefore, it is very necessary to find novel treatment options with a good prognosis for the treatment or prevention of GBM. In recent years, flavonoids are frequently used to treat cancer. It is a new attractive molecule that may achieve this promising treatment option. Flavonoids have been proved to have many biological functions, such as antioxidation, prevention of angiogenesis, anti-inflammation, inhibition of cancer cell proliferation, and protection of nerve cells. It has also shown the ability to regulate long non-coding RNA (LncRNA). Studies have confirmed that flavonoids can regulate epigenetic modification, transcription, and change microRNA (miRNA) expression of GBM through lncRNA at the gene level. It also found that flavonoids can induce apoptosis and autophagy of GBM cells by regulating lncRNA. Moreover, it can improve the metabolic abnormalities of GBM, interfere with the tumor microenvironment and related signaling pathways, and inhibit the angiogenesis of GBM cells. Eventually, flavonoids can block the tumor initiation, growth, proliferation, differentiation, invasion, and metastasis. In this review, we highlight the role of lncRNA in GBM cancer progression and the influence of flavonoids on lncRNA regulation. And emphasize their expected role in the prevention and treatment of GBM., Competing Interests: Conflict of interest statement We declare that we have no financial and personal relationships with other people ororganizations that can inappropriately influence our work, there is no professional or otherpersonal interest of any nature or kind in any product, service and/or company that could beconstrued as influencing the position presented in, or the review of, the manuscript entitled., (Copyright © 2023. Published by Elsevier Masson SAS.)

Non-coding RNA (ncRNA) is a special type of RNA transcript that makes up more than 90 % of the human genome. Although ncRNA typically does not encode proteins, it indirectly controls a wide range of biological processes, including cellular metabolism, development, proliferation, transcription, and post-transcriptional modification. NcRNAs include small interfering RNA (siRNA), PIWI-interacting RNA (piRNA), tRNA-derived small RNA (tsRNA), etc. The most researched of these are miRNA, lncRNA, and circRNA, which are crucial regulators in the onset of diabetes and the development of associated consequences. The ncRNAs indicated above are linked to numerous diabetes problems by binding proteins, including diabetic foot (DF), diabetic nephropathy, diabetic cardiomyopathy, and diabetic peripheral neuropathy. According to recent studies, Mir-146a can control the AKAP12 axis to promote the proliferation and migration of diabetic foot ulcer (DFU) cells, while lncRNA GAS5 can activate HIF1A/VEGF pathway by binding to TAF15 to promote DFU wound healing. However, there are still many unanswered questions about the mechanism of action of ncRNAs. In this study, we explored the mechanism and new progress of ncRNA-protein binding in DF, which can provide help and guidance for the application of ncRNA in the early diagnosis and potential targeted intervention of DFU., Competing Interests: Conflict of interest statement The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

LncRNAs are involved in many physiological and pathological processes, including chromatin remodeling, transcription, posttranscriptional gene expression, mRNA stability, translation, and posttranslational modification, and their functions depend on subcellular localization. MIR503HG is a lncRNA as well as a host gene for the miRNAs miR-503 and miR-424. MIR503HG functions independently or synergistically with miR-503. MIR503HG affects cell proliferation, invasion, metastasis, apoptosis, angiogenesis, and other biological behaviors. The mechanism of MIR503HG in disease includes interaction with protein, sponging miRNA to regulate downstream target gene, and participation in NF-κB, TGF-β, ERK/MAPK, and PI3K/AKT signaling pathways. In this review, we summarize the molecular mechanisms of MIR503HG in disease and its potential applications in diagnosis, prognosis, and treatment. We also raise some unanswered questions in this area, providing insights for future research., Competing Interests: Declaration of Interest We declare that we have no financial and personal relationships with other people or organizations that can inappropriately influence our work. We declare that the authors have no competing interests., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Placental complication arises due to various risk factors occurring during the pregnancy period, leading to an increased morbidity rate. Placenta related disorders are one of primary reason for pregnancy related complications and the clinical incidences are seen to be on the rise. Most of the common disorders associated with placenta are pre-eclampsia, recurrent spontaneous abortions, intra-uterine growth restriction etc. Several studies have been done to understand the genetics and immunological attributes leading to the development of placenta associated complications. In the recent years, studies were able to establish and identify ncRNAs found specifically in foetal tissues such as the placenta. The aberrant expression patterns of ncRNA associated with placenta has been linked to disorders such as pre-eclampsia. Since ncRNA play a major role in regulating biological processes like trophoblast growth, migration and invasion, their aberrant expression could very well lead to complications like spontaneous pregnancy loss. This review article focuses on the association of ncRNAs - miRNAs, lncRNAs, CircRNAs in placenta associated complications as well as the different ncRNA based therapies. Deciphering the exact mechanism involved in the regulation and development of placenta through ncRNA will help in using it as a biomarker for early diagnosis. Understanding the therapeutic opportunities of ncRNAs in placental disorders will result in better treatment strategies., Competing Interests: Conflict of interest statement The authors declare that they have no known competing for financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Increasing evidence suggests that long non-coding RNAs (lncRNAs) are closely related to the initialization and development of human diseases. lncRNA just proximal to XIST (JPX), as a newly identified lncRNA, has been reported to be aberrantly expressed and associated with pathophysiological traits in numerous diseases, particularly cancers. More importantly, JPX has been proven to play important roles in various biological functions, including cell proliferation, migration, invasion, apoptosis, chemoresistance, and differentiation. In addition, we discuss the diverse molecular mechanisms and correlation with RNA methylation of JPX in several cancers. In this Review, we summarize current studies on JPX's roles in diseases and its potential application as a biomarker for both diagnoses and prognoses and a therapeutic target in human diseases., Competing Interests: Conflict of interest statement The authors declare no competing interests., (Copyright © 2022 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Epigenetic factors are critical regulators of biological and pathological mechanisms and they could interact with different molecular pathways. Targeting epigenetic factors has been an idea approach in disease therapy, especially cancer. Accumulating evidence has highlighted function of long non-coding RNAs (lncRNAs) as epigenetic factors in cancer initiation and development and has focused on their association with downstream targets. microRNAs (miRNAs) are the most well-known targets of lncRNAs and present review focuses on lncRNA-miRNA axis in malignancy and therapy resistance of tumors. LncRNA-miRNA regulates cell death mechanisms such as apoptosis and autophagy in cancers. This axis affects tumor metastasis via regulating EMT and MMPs. Besides, lncRNA-miRNA axis determines sensitivity of tumor cells to chemotherapy, radiotherapy and immunotherapy. Based on the studies, lncRNAs can be affected by drugs and genetic tools in cancer therapy and this may affect expression level of miRNAs as their downstream targets, leading to cancer suppression/progression. LncRNAs have both tumor-promoting and tumor-suppressor functions in cancer and this unique function of lncRNAs has complicated their implication in tumor therapy. LncRNA-miRNA axis can also affect other signaling networks in cancer such as PI3K/Akt, STAT3, Wnt/β-catenin and EZH2 among others. Notably, lncRNA/miRNA axis can be considered as a signature for diagnosis and prognosis in cancers., Competing Interests: Competing interests The authors declare no conflict of interest., (Copyright © 2022. Published by Elsevier Masson SAS.)

Gastric cancer (GC) is one of the most common gastrointestinal malignancies in the world. Growing evidence emphasizes the critical role of long non-coding RNA (lncRNA) in GC tumorigenesis. The aim of the research was to elucidate the effect and mechanism of Babao Dan (BBD) on lymphangiogenesis of GC in vitro and in vivo via lncRNA-ANRIL/VEGF-C/VEGFR-3 signaling axis. The present study investigated BBD significantly decreased the expression of lncRNA-ANRIL and VEGF-C in GC cells (AGS, BGC823, and MGC80-3) by using real-time quantitative polymerasechain reaction (RT-qPCR) and the secretion and expression of VEGF-C by (enzyme linked immunosorbent assay) ELISA and western blot (WB). BBD significantly inhibited the tumor xenograft of GC growth and the expression of lncRNA-ANRIL, VEGF-C, VEGFR-3 and LYVE-1 in vivo. BBD reduced serum VEGF-C level. In vitro, BBD inhibited the tube formation and decreased the cell viability, proliferation and migration of HLECs by using tube formation, MTT, Hoechst and Transwell assays. In addition, WB assay found that BBD decreased the expression levels of VEGF-C, VEGFR-3, matrix metallopeptidase 2 (MMP-2) and matrix metallopeptidase 9 (MMP-9), and RT-qPCR assay found that the mRNA expression levels of lncRNA-ANRIL, VEGF-C, VEGFR-3, MMP-2, MMP-9, CDK4, Cyclin D1, and Bcl-2 were down-regulated, and the expression of p21 and Bax were increased. Taken together, these results demonstrated that BBD inhibited lymphangiogenesis of GC in vitro and in vivo via the lncRNA-ANRIL/VEGF-C/VEGFR-3 signaling axis., Competing Interests: Conflict of interest statement The authors disclose no conflicts of interest regarding this study., (Copyright © 2022. Published by Elsevier Masson SAS.)

Abnormal expression of long non-coding RNAs (lncRNAs) plays an essential role in various malignant neoplasia. As a newly identified lncRNA, LINC01234 is abnormally expressed in several types of cancers and promotes the development of cancers. Accumulating evidence indicates that overexpression of LINC01234 is associated with poor clinical outcomes. Moreover, LINC01234 modulates many cellular events as a putative proto-oncogene, including proliferation, migration, invasion, apoptosis, cell cycle progression, and EMT. In terms of molecular mechanism, LINC01234 regulates gene expression by acting as ceRNA, participating in signaling pathways, interacting with proteins and other molecules, and encoding polypeptide. It reveals that LINC01234 may serve as a potential biomarker for cancer diagnosis, treatment, and prognosis. This review summarizes the expression pattern, biological function, and molecular mechanism of LINC01234 in human cancer and discusses its potential clinical utility., Competing Interests: Conflict of interest statement The authors declare that there is no conflict of interest., (Copyright © 2022 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Long non-coding RNAs (lncRNAs) play a critical role in several human diseases, particularly in solid tumors. Specific lncRNAs are effective biological molecular markers for diagnosing diseases and determining patient prognosis for designing molecularly targeted therapies. HOTAIR is reportedly involved in several physiological emerging processes in solid tumor, such as unlocking phenotypic plasticity, polymorphic microbiome, and cellular senescence, and has been implicated in tumorigenesis and progression. This review summarizes the relationship between the levels of expression, biological features, clinical symptoms, and regulatory mechanisms of HOTAIR action in solid cancers and discusses the clinical applicability of HOTAIR as a biomarker for predicting risk, diagnosis, prognosis, and designing targeted therapy for cancer., Competing Interests: Conflict of interest statement This manuscript has been read and approved by all authors and all declare that they have no competing interests., (Copyright © 2022 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Osteoarthritis (OA) is a degenerative disease associated with joint inflammation, articular cartilage degeneration and subchondral hypertrophy. Small molecules which both ameliorate chondrocyte OA phenotype and activate bone marrow-derived mesenchymal stem cells (BMSCs) chondrogenesis under inflammatory conditions have the therapeutical potential for OA treatment. In this study, we characterized a novel small molecule which could ameliorate OA progression via novel regulating mechanisms. Docosahexaenoic acid (DHA), a bioactive molecule, was screened from a small molecule library and showed anti-inflammatory and chondroprotective effects in OA chondrocytes, as well as ameliorated IL-1β impaired BMSCs chondrogenesis in Wnt/β-catenin and NF-κB signaling dependent manners. Furthermore, Malat1 was found to be the key mediator of DHA-mediating anti-inflammation chondroprotection and chondrogenesis. DHA also rescued cartilage loss and damage in a surgery-induced OA mice model. The elevation of serum Malat1 levels caused by OA was also downregulated by DHA treatment. Taken together, our findings demonstrated that DHA, with a dual-signaling repression property, exerted its anti-inflammation, chondroprotection and chondrogenesis function possibly via regulating Malat1 level, suggesting that it may be a possible drug candidate for OA patients with elevated MALAT1 expression levels., Competing Interests: Conflict of interest statement The authors declared no conflict of interests., (Copyright © 2022 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Injuries caused by cerebral ischemia reperfusion (CIR) can worsen neurological outcomes, Biliverdin (BV) is an antioxidant and anti-apoptotic agent that was shown to affect CIR, although the underlying mechanisms remain unclear. In this study, we investigated the role of BV and its potential underlying mechanism in CIR injury. CIR rat models and primary cortical neurons were established and treated with and without BV. Additionally, adenovirus vectors that could overexpress LncRNA H19 and overexpress or knock-down miR-181b-5p and Esm1 were created to investigate their regulation of molecular expression. Our findings showed that BV could significantly improve CIR injury, both in vivo and in vitro, decrease LncRNA H19 and Esm1 expression, and increase miR-181b-5p expression. Overexpression of LncRNA H19 inhibited the anti-injury effects of BV. Further, the down-regulation of miR-181b-5p or up-regulation of Esm1 expression weakened the in vitro protective effect of BV. RNA immunoprecipitation assay and dual luciferase reporter gene assay further confirmed that LncRNA H19 could sponge miR-181b-5p, and Esm1 was the target of miR-181b-5p. Rescue experiments confirmed that BV could regulate the LncRNA H19/miR-181b-5p/Esm1 molecular axis. Lastly, proteomic and bioinformatic analyzes revealed that Esm1 upregulation in BV-treated neurons resulted in the differential expression of 16 proteins, including 9 upregulated and 7 downregulated proteins. In conclusion, this study found that BV could ameliorate CIR injury by regulating the LncRNA H19/miR-181b-5p/Esm1 axis., Competing Interests: Conflict of interest statement All authors have claimed no conflict of interests in this research., (Copyright © 2022 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Long non-coding RNAs (LncRNAs) are involved in several types of cancer and participate actively in tumorigenesis and disease progression. LncRNA FTX is the transcription product of the FTX gene located at the X-inactivation center (Xic). LncRNA FTX has been shown to regulate cancer cell proliferation, migration, and aberrant metabolism, as well as increase tumor growth and metastasis in vivo. Herein, we summarized currently available research on the interaction between LncRNA FTX and associated molecules and signaling pathways in malignant tumors to better understand the biological roles of LncRNA FTX in cancer progression., (Copyright © 2022 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Hepatocellular carcinoma is one of the most common highly malignant tumors in humans, as well as the leading cause of cancer-related death worldwide. Growing evidence has indicated that lncRNAs are implicated in different molecular mechanisms, including interactions with DNA, RNA, or protein, so that to regulate the gene expression at epigenetic, transcriptional, or posttranscriptional level. Moreover, the mechanism of action of lncRNA is closely related to its subcellular localization. An increasing number of studies have certified that lncRNA plays a significant biological function in the occurrence and development of hepatocellular carcinoma, such as involving in cell proliferation, metastasis, apoptosis, ferroptosis, autophagy, and reprogramming of energy metabolism. As a result, lncRNA has great potential as a novel biomarker for diagnosis or therapeutics of hepatocellular carcinoma. In this review, we highlight the correlation between subcellular localization of lncRNA and its mechanism of action, discuss the biological roles of lncRNA and the latest research advances in hepatocellular carcinoma, and emphasize the potential of lncRNA as a therapeutic target for advanced patients of hepatocellular carcinoma., (Copyright © 2022 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

LINC00461 is located in the intergenic region between the protein-coding genes MEF2C and TMEM161B. LINC00461 upregulation was associated with the risk of 13 tumors and was strongly associated with clinicopathologic features and poor prognosis in 11 tumors. LINC00461 is involved in resistance to four anticancer drugs, including sunitinib for renal cell carcinoma, cisplatin for head and neck squamous cell carcinoma and rectal cancer, temozolomide for glioma, and docetaxel for breast cancer. LINC00461 can sponge 18 miRNAs to form a complex ceRNA network that regulates the expression of a large number of downstream genes. LINC00461 is involved in the MAPK/ERK signaling pathway and PI3K/AKT signaling pathway, thereby promoting tumorigenesis. Notably, knockdown of LINC00461 in exosomes antagonizes tumor cell proliferation in multiple myeloma. This article summarizes the diagnostic, prognostic, and therapeutic value of LINC00461 in various tumors, and systematically describes the ceRNA network and signaling pathways associated with LINC00461, providing potential directions for future LINC00461 research., (Copyright © 2022 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Background/aims: Arsenic trioxide (ATO) is an effective anti-cancer drug. Nonetheless, it possesses cardiotoxic effects which limit its clinical application. The present study aims to elucidate the molecular basis of ATO-induced cardiotoxicity through using whole transcriptome analysis., Methods: The whole transcriptome in ATO-treated mice myocardium was analyzed using RNA sequencing technique. These results were confirmed by real-time PCR. The lncRNA-mRNA and circRNA-mRNA co-expression networks were constructed. Finally, a circRNA-lncRNA co-regulated competing endogenous RNA (ceRNA) network was constructed. GO and KEGG pathway analyses were performed. The expression levels of Txnip and Spp1 in ATO-treated neonatal mouse cardiomyocytes were validated by real-time PCR., Results: A total of 113 mRNAs, 159 lncRNAs, 35 miRNAs, and 94 circRNAs were differentially expressed in ATO-treated mice myocardium. A lncRNA-circRNA co-regulation network was constructed. Function annotation revealed that aberrantly expressed genes may be enriched in the 'Wnt signaling pathway', 'Hippo signaling pathway', 'Notch signaling pathway', etc. Finally, the expression levels of Txnip and Spp1 were validated in ATO-treated cardiomyocytes, which was in accordance with the RNA-sequencing results., Conclusion: ATO altered coding and noncoding RNA profiles in myocardium of mice. The ATO-related lncRNA-circRNA co-regulation network was constructed. Genes in the co-regulation network are likely to play important roles in the cardiotoxicity of ATO. This study provides new insights into the prevention and treatment of ATO-induced cardiotoxicity., (Copyright © 2022. Published by Elsevier Masson SAS.)