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Abstract Metastasis accounts for almost 90% of breast cancer-related fatalities, making it frequent malignancy and the main reason of tumor mortality globally among women. LSD1 is a histone demethylase, which plays an important role in breast cancer. In order to explore the effect of LSD1 on invasion and migration of breast cancer, we treated breast cancer cells with MCF7 and T47D exosomes knocked down by LSD1, and the invasion and migration of breast cancer cells were significantly enhanced. This phenomenon indicates that LSD1 can inhibit the invasion and migration of breast cancer cells. miR-1290 expression was downregulated in LSD1 knockdown MCF7 exosomes. By analyzing the database of miR-1290 target gene NAT1, we verified that miR-1290 could regulate the expression of NAT1. These data provide fresh insights into the biology of breast cancer therapy by demonstrating how the epigenetic factor LSD1 stimulates the breast cancer cells’ invasion and migration via controlling exosomal miRNA.

Metastasis accounts for almost 90% of breast cancer-related fatalities, making it frequent malignancy and the main reason of tumor mortality globally among women. LSD1 is a histone demethylase, which plays an important role in breast cancer. In order to explore the effect of LSD1 on invasion and migration of breast cancer, we treated breast cancer cells with MCF7 and T47D exosomes knocked down by LSD1, and the invasion and migration of breast cancer cells were significantly enhanced. This phenomenon indicates that LSD1 can inhibit the invasion and migration of breast cancer cells. miR-1290 expression was downregulated in LSD1 knockdown MCF7 exosomes. By analyzing the database of miR-1290 target gene NAT1, we verified that miR-1290 could regulate the expression of NAT1. These data provide fresh insights into the biology of breast cancer therapy by demonstrating how the epigenetic factor LSD1 stimulates the breast cancer cells' invasion and migration via controlling exosomal miRNA. [ABSTRACT FROM AUTHOR]

Background & Objective: This study aimed to determine the incidence of microRNA (miRNA; miR-1290) in the serum of oral squamous cell carcinoma (OSCC) patients compared to a control group using the qualitative real-time polymerase chain reaction (PCR) method. Methods: Blood serum samples were obtained from patients diagnosed with OSCC and confirmed through biopsy. The samples were collected from patients referred to the Mashhad Dental Faculty and Ghaem Hospital. The OSCC group consisted of 17 patients, while the healthy group included 15 individuals. RNA was extracted from the patient samples, and samples with an A260/280 ratio between 1.8 and 2.0 (indicating acceptable RNA quality) were immediately converted into complementary DNA (cDNA) using albumin and cDNA reference genes. The SYBR green real-time reverse transcriptase PCR method was used to measure the presence of miR-1290 in the blood samples. Results: A total of 32 patients were examined in this study, including 17 women (53.1%) and 15 men (46.9%). The mean age was 46.7 years in the healthy group and 54.6 years in the SCC group, indicating a significant difference (P<0.05). The expression level of the miR-1290 gene was higher in patients with SCC compared to the healthy group (P=0.000). While the expression level of miR-1290 was higher in grade 3 and advanced stage than in grades 2 and 1 and early stage, the differences were not statistically significant (P=0.173 and P=0.564 for grade and stage, respectively). Conclusion: The expression level of miR-1290 may increase in SCC patients compared to healthy individuals, making it a potential circulating biomarker. Further investigations for diagnostic utility would be warranted. [ABSTRACT FROM AUTHOR]

Abstract Despite receiving first-line treatment, ovarian cancer patients continue to experience a high rate of recurrence; nearly all women with ovarian cancer develop chemoresistance and succumb to the disease. In this study, cancer-associated fibroblasts (CAFs) and normal fibroblasts (NFs) were isolated from tumor-containing and normal omenta, respectively, and the downregulation of osteoglycin (OGN) in CAFs was observed. OGN overexpression in CAFs significantly inhibited ovarian cancer cell viability, DNA synthesis, and cell invasion. OGN overexpression also changed epithelial-mesenchymal transition (EMT) markers and promoted mTOR and Akt phosphorylation in ovarian cancer cells. miR-1290 targeted OGN and inhibited OGN expression. miR-1290 overexpression in CAFs significantly promoted ovarian cancer cell viability, DNA synthesis, and cell invasion. Moreover, miR-1290 overexpression in CAFs also changed EMT markers and promoted mTOR and Akt phosphorylation within ovarian carcinoma cells. Finally, when ovarian cancer cells in a conditioned medium derived from CAFs co-transduced with miR-1290 mimics and OGN-OE were cultured, the effects of miR-1290 overexpression were partially reversed by OGN overexpression. In nude mouse xenograft tumor models, OGN overexpression in CAFs suppressed tumor growth, whereas miR-1290 overexpression in CAFs increased tumor growth. In conclusion, a miRNA/mRNA axis in ovarian cancer CAFs modulating the proliferative and invasive abilities of ovarian cancer cells, possibly via the Akt/mTOR pathway, was demonstrated.

Abstract Background Exosomes are critical mediators of tumor cell‐microenvironment cross talk. However, the mechanisms by which hypoxic Lung adenocarcinoma (LUAD)‐derived exosomes modulate macrophage polarization remain largely unknown. The aim of this study was to investigate the effects of hypoxic LUAD‐derived exosome on macrophage polarization and explore the underlying molecular mechanism. Materials and methods LUAD‐derived exosomes were isolated, and then confirmed by transmission electron microscopy, nanoparticle tracking analysis, and Western blot. Internalization of exosomes in macrophages was detected by confocal microscope. Gain‐ and loss‐of‐function experiments, rescue experiments, and xenograft models were performed to uncover the underlying mechanisms of exosomal miR‐1290 induced macrophage polarization in vitro and in vivo. Results miR‐1290 was enriched in hypoxic LUAD cancer cell‐derived exosomes and could be transferred to macrophages. Overexpression of miR‐1290 in macrophages‐induced polarization of M2 phenotype. Luciferase assay verified SOCS3 was the target of miR‐1290. Hypoxic LUAD cell‐derived exosomal miR‐1290 activated the STAT3 signaling pathway by targeting SOCS3 to promote M2 macrophage polarization. Conclusion Hypoxic LUAD cells generate miR‐1290‐rich exosomes that promote M2 polarization of macrophages. Targeting exosomal miR‐1290 may provide a potential immunotherapeutic strategy for LUAD.

Background: Enhancing the diagnostic efficacy of early-stage lung cancer is crucial for improving prognosis. The objective of this study was to ascertain dependable exosomal miRNAs as biomarkers for the diagnosis of lung cancer. Methods: Exosomal miRNA candidates were identified through miRNA sequencing and subsequently validated in various case-control sets using real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR). The correlation between the expression of exosomal miRNAs and the clinicopathological features of lung cancer was investigated. To assess the diagnostic efficacy of exosomal miRNAs for lung cancer, the receiver operating characteristic (ROC) curve analysis was conducted. The optimal cutoff value of exosomal miRNAs was determined in the testing cohort and subsequently confirmed in the validation cohort. Results: The results showed that the expression of exosomal miR-1290 was significantly elevated, while that of miR-29c-3p was significantly decreased in the plasma of lung cancer patients, especially in those with early-stage lung cancer, compared to individuals with benign lung conditions (P

MicroRNAs are a set of small non-coding RNAs that could change gene expression with post-transcriptional regulation. MiRNAs have a significant role in regulating molecular signaling pathways and innate and adaptive immune system activity. Moreover, miRNAs can be utilized as a powerful instrument for tissue engineers and regenerative medicine by altering the expression of genes and growth factors. MiR-1290, which was first discovered in human embryonic stem cells, is one of those miRNAs that play an essential role in developing the fetal nervous system. This review aims to discuss current findings on miR-1290 in different human pathologies and determine whether manipulation of miR-1290 could be considered a possible therapeutic strategy to treat different non-malignant diseases. The results of these studies suggest that the regulation of miR-1290 may be helpful in the treatment of some bacterial (leprosy) and viral infections (HIV, influenza A, and Borna disease virus). Also, adjusting the expression of miR-1290 in non-infectious diseases such as celiac disease, necrotizing enterocolitis, polycystic ovary syndrome, pulmonary fibrosis, ankylosing spondylitis, muscle atrophy, sarcopenia, and ischemic heart disease can help to treat these diseases better. In addition to acting as a biomarker for the diagnosis of non-malignant diseases (such as NAFLD, fetal growth, preeclampsia, down syndrome, chronic rhinosinusitis, and oral lichen planus), the miR-1290 can also be used as a valuable instrument in tissue engineering and reconstructive medicine. Consequently, it is suggested that the regulation of miR-1290 could be considered a possible therapeutic target in the treatment of non-malignant diseases in the future. [ABSTRACT FROM AUTHOR]

Background: Exosomes are critical mediators of tumor cell‐microenvironment cross talk. However, the mechanisms by which hypoxic Lung adenocarcinoma (LUAD)‐derived exosomes modulate macrophage polarization remain largely unknown. The aim of this study was to investigate the effects of hypoxic LUAD‐derived exosome on macrophage polarization and explore the underlying molecular mechanism. Materials and methods: LUAD‐derived exosomes were isolated, and then confirmed by transmission electron microscopy, nanoparticle tracking analysis, and Western blot. Internalization of exosomes in macrophages was detected by confocal microscope. Gain‐ and loss‐of‐function experiments, rescue experiments, and xenograft models were performed to uncover the underlying mechanisms of exosomal miR‐1290 induced macrophage polarization in vitro and in vivo. Results: miR‐1290 was enriched in hypoxic LUAD cancer cell‐derived exosomes and could be transferred to macrophages. Overexpression of miR‐1290 in macrophages‐induced polarization of M2 phenotype. Luciferase assay verified SOCS3 was the target of miR‐1290. Hypoxic LUAD cell‐derived exosomal miR‐1290 activated the STAT3 signaling pathway by targeting SOCS3 to promote M2 macrophage polarization. Conclusion: Hypoxic LUAD cells generate miR‐1290‐rich exosomes that promote M2 polarization of macrophages. Targeting exosomal miR‐1290 may provide a potential immunotherapeutic strategy for LUAD. [ABSTRACT FROM AUTHOR]

Circular RNAs (CircRNAs) are reported to exert vital regulatory roles in the occurrence and development of various human malignancies, including non-small cell lung cancer (NSCLC). Bioinformatics methods identified the down-regulation of circSCN8A (circBase ID: hsa_circ_0026337) in NSCLC tissues. However, its biological functions and molecular mechanisms in NSCLC remain unknown. In this study, we found that circSCN8A expression was down-regulated in NSCLC tissues and cells. Low circSCN8A expression was positively associated with aggressive clinicopathological characteristics and poor prognosis in NSCLC patients. CircSCN8A suppressed cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro and blocked tumor growth in vivo. Moreover, circSCN8A promoted cell ferroptosis in NSCLC. Mechanistically, circSCN8A acted as a competing endogenous RNA (ceRNA) by sponging miR-1290 to enhance the expression of long-chain acyl-CoA synthetase-4 (ACSL4). Furthermore, the knockdown of ACSL4 or overexpression of miR-1290 reversed the effect of circSCN8A on facilitating ferroptosis and inhibiting cell proliferation and metastasis. In summary, circSCN8A represses cell proliferation and metastasis in NSCLC by regulating the miR-1290/ACSL4 axis to induce ferroptosis. Thus, circSCN8A may represent a promising therapeutic target against NSCLC. [ABSTRACT FROM AUTHOR]

Introduction: Colorectal cancer (CRC) is the third most common cancer in the world with high mortality, hence, understanding the molecular mechanisms involved in the tumor progression are important for CRC diagnosis and treatment. MicroRNAs (miRNAs) are key gene expression regulators that can function as tumor suppressors or oncogenes in tumor cells, and modulate angiogenesis as a critical process in tumor metastasis. MiR-1290 has been demonstrated as an onco-miRNA in various types of cancer, however, the role of miR-1290 in CRC is not fully understood. This study aimed to investigate the oncogenic and angiogenic potential of miR-1290 in CRC. Methods: Lenti-miR-1290 was transduced into HCT116, SW480, and human umbilical vein endothelial cells (HUVECs). By bioinformatics analysis, we identified thrombospondin 1 (THBS1) as a novel predicted target for miR-1290. Quantitative real-time PCR, western blotting, and luciferase reporter assay were used to demonstrate suppression of miR-1290 target genes including THBS1, Dickkopf Wnt signaling pathway inhibitor 3 (DKK3), and suppressor of cancer cell invasion (SCAI) in HCT116 and HUVECs. Cell cycle analysis, proliferation, migration and, tube formation were determined by flow cytometry, MTT, wound healing, and tube formation assays, respectively. Results: MiR-1290 significantly decreased the expression of THBS1, DKK3, and SCAI. We demonstrated that miR-1290 enhanced proliferation, migration, and angiogenesis partially through suppression of THBS1, DKK3, and SCAI in CRC. Conclusion: These results suggest a novel function of miR-1290 which may contribute to tumorigenesis and angiogenesis in CRC.

Abstract Background Circular RNAs (circRNAs) can function as competing endogenous RNAs (ceRNAs) to impact the development of esophageal squamous cell cancer (ESCC). Human circ_0001946 has been identified as a potential anticancer factor in ESCC, yet our understanding of its molecular basis remains limited. Methods Circ_0001946, microRNA (miR)‐1290 and SRY‐box transcription factor 6 (SOX6) were quantified by quantitative reasl‐time PCR (qRT‐PCR) or immunoblotting. Cell proliferation was assessed by CCK‐8 and EDU assays. Cell apoptosis and invasion were evaluated by flow cytometry and transwell assays, respectively. Cell migration was detected by transwell and wound‐healing assays. The direct relationship between miR‐1290 and circ_0001946 or SOX6 was determined by dual‐luciferase reporter and RNA immunoprecipitation (RIP) assays. Xenograft model assays were used to assess the role of circ_0001946 in tumor growth. Results Circ_0001946 expression was attenuated in human ESCC, and circ_0001946 increase impeded cell proliferation, invasion, migration and enhanced apoptosis in vitro. Moreover, circ_0001946 increase diminished xenograft growth in vivo. Mechanistically, circ_0001946 bound to miR‐1290, and re‐expression of miR‐1290 reversed circ_0001946‐dependent cell properties. SOX6 was a miR‐1290 target and it was responsible for the regulation of miR‐1290 in cell properties. Furthermore, circ_0001946 functioned as a ceRNA to regulate SOX6 expression via miR‐1290. Conclusion Our findings uncover an undescribed molecular mechanism, the circ_0001946/miR‐1290/SOX6 ceRNA crosstalk, for the anti‐ESCC activity of circ_0001946.

Communication between the maternal uterus and the embryo is vital for a successful pregnancy. Exosomes, subtypes of extracellular vesicles comprising many bioactive factors, regulate the early stages of pregnancy, specifically during embryo implantation. Nevertheless, the mechanism by which exosomal microRNAs (miRNAs) derived from placental trophoblasts regulate embryo implantation remains elusive. We isolated and identified exosomes derived from placental trophoblast cells (HTR8/SVneo). Subsequently, we evaluated the loading miRNA in exosomes by small RNA sequencing. Consequently, we showed that trophoblast cell-derived exosomes could transfer to endometrial epithelial cells. Besides, these exosomes promoted the epithelial-mesenchymal transition (EMT) as well as migration of endometrial cells and were implicated in the regulation of inflammation. Further, the specific miRNAs were screened in exosomes, and as a result, miRNA (miR)-1290 was enriched specifically in exosomes. miR-1290 promoted the expression of inflammatory factors (interleukin [IL]-6 and IL-8) and migration of endometrial epithelial cells. In addition, exosomal miR-1290 promoted angiogenesis in vitro. More importantly, by targeting LHX6, trophoblast HTR8/SVneo cell-derived exosomal miR-1290 promoted the EMT process of endometrial epithelial cell HEC-1-A. Altogether, our findings provide novel insights into the mechanism of trophoblast cell-derived exosomes during embryo implantation.

Purpose: To explore the roles and underlying mechanisms of miR-1290 in determining the sensitivity of triple-negative breast cancer (TNBC) to radiation therapy. Methods: ELISA was performed to detect the levels of IL-18 and IL-1β in radiosensitive cells and serum samples. The level of miR-1290 in radiosensitive cells and tissues was assessed by qRT–PCR assay. A luciferase reporter assay was performed to confirm NLRP3 as the target of miR-1290. Functionally, the roles of miR-1290 in TNBC radioresistance were analyzed by transfection of either miR-1290 mimic or miR-1290 inhibitor. Moreover, the involvement of the miR-1290/NLRP3 axis in TNBC radioresistance was analyzed by experiments with a miR-1290 mimic and NLRP3 overexpression. MTT and colony formation assays were used to detect radiation-induced cell viability and proliferation. qRT–PCR and western blot assays were used to detect pyroptosis markers (NLRP3, ACS and caspase-1). Results: The results showed that radioresistance in TNBC cells was associated with a reduction in pyroptosis. miR-1290 expression was increased in radioresistant cells, and it had higher expression levels in the radioresistant tumor tissues of TNBC patients compared to the radiosensitive samples. The miR-1290 mimic suppressed radiation-induced pyroptosis and reduced the radiosensitivity of TNBC cells. Moreover, we found that NLRP3 was a potential target of miR-1290. Overexpression of NLRP3 partly reversed the effects of miR-1290 on pyroptosis and radioresistance. The mouse models showed that miR-1290 suppressed tumor size, tumor weight and pyroptosis. Conclusions: miR-1290/NLRP3-mediated pyroptosis may play an important role in determining radioresistance in TNBC and serve as a novel therapeutic option. [ABSTRACT FROM AUTHOR]

To explore the expression of serum miR-1290 in the patients with colorectal cancer (CRC) and its relationship with clinicopathological characteristics,and to analyze the diagnostic value of miR-1290 combined with carcinoembryonic antigen (CEA) detection in CRC.Methods The serum samples of 80 patients with CRC,40 patients with colorectal adenomas (CRA) and 40 health controls from January 2017 to December 2019 in Yichuan County People's Hospital were collected.Quantitative real-time PCR (qPCR) and electrochemical reflection (ECL) were used to detect the expression of serum miR-1290 and CEA in three groups of subjects.Chi-square test was used to analyze the relationship between miR-1290 expression, CEA expression and clinicopathological characteristics in CRC patients.Receiver operating characteristic curve (ROC) was used to analyze the diagnostic values of miR-1290 alone or in combination with CEA detection for CRC.Results The expression of serum miR-1290 or CEA in CRC patients were higher than those in CRA patients or healthy controls.The differences were statistically significant (P <0.05).The expression of miR- 1290 in serum of CRC patients was closely correlated with the TNM stage,tumor differentiation and distant metastasis (P <0.05).And the expression of CEA was closely correlated with the TNM stage and tumor differentiation (P <0.05).The area under the curve (AUC) of miR-1290 for the diagnosis of CRC was 0.807 (95%CI 0.863-0.951).And the specificity and sensitivity were 71.2% and 80.1%,respectively.The miR- 1290 combined with CEA detection could further improve the diagnostic efficiency.The AUC increased to 0.840 (95%CI 0.907-0.973).The diagnostic sensitivity and specificity were 88.8% and 85.2%,respectively. Conclusion The high expression of miR-1290 in the serum of CRC patients is correlated with clinicopathological features.The detection of serum miR-1290 combined with CEA has preferable diagnostic value for CRC diagnosis. [ABSTRACT FROM AUTHOR]

Introduction: Colorectal cancer (CRC) is the third most common cancer in the world with high mortality, hence, understanding the molecular mechanisms involved in the tumor progression are important for CRC diagnosis and treatment. MicroRNAs (miRNAs) are key gene expression regulators that can function as tumor suppressors or oncogenes in tumor cells, and modulate angiogenesis as a critical process in tumor metastasis. MiR-1290 has been demonstrated as an onco-miRNA in various types of cancer, however, the role of miR-1290 in CRC is not fully understood. This study aimed to investigate the oncogenic and angiogenic potential of miR-1290 in CRC. Methods: Lenti-miR-1290 was transduced into HCT116, SW480, and human umbilical vein endothelial cells (HUVECs). By bioinformatics analysis, we identified thrombospondin 1 (THBS1) as a novel predicted target for miR-1290. Quantitative real-time PCR, western blotting, and luciferase reporter assay were used to demonstrate suppression of miR-1290 target genes including THBS1, Dickkopf Wnt signaling pathway inhibitor 3 (DKK3), and suppressor of cancer cell invasion (SCAI) in HCT116 and HUVECs. Cell cycle analysis, proliferation, migration and, tube formation were determined by flow cytometry, MTT, wound healing, and tube formation assays, respectively. Results: MiR-1290 significantly decreased the expression of THBS1, DKK3, and SCAI. We demonstrated that miR-1290 enhanced proliferation, migration, and angiogenesis partially through suppression of THBS1, DKK3, and SCAI in CRC. Conclusion: These results suggest a novel function of miR-1290 which may contribute to tumorigenesis and angiogenesis in CRC. [ABSTRACT FROM AUTHOR]

Abstract Background Sevoflurane (Sev) has been reported to inhibit cancer development, and sevoflurane treatment in cancers is implicated with the deregulation of specific non-coding RNAs (ncRNAs). This study aimed to investigate the relationship between sevoflurane and circular RNA reelin (circRELN) in glioma. Methods The expression of circRELN, microRNA-1290 (miR-1290) and RAR-related orphan receptor A (RORA) was measured by quantitative real-time PCR (qPCR). Cell proliferative capacity was assessed by cell counting kit-8 (CCK-8) and colony formation assays. Cell apoptosis and cell cycle distribution were monitored by flow cytometry assay. Cell migration was assessed by wound healing assay and transwell assay, and cell invasion was assessed by transwell assay. The protein levels of matrix metalloproteinase-2 (MMP2), MMP9 and RORA were quantified by western blot. Tumor growth in vivo was assessed by Xenograft models. The binding relationship between miR-1290 and circRELN or RORA was verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Results We found that circRELN expression was declined in glioma tissues and cells, while Sev treatment enhanced circRELN expression. In function, Sev notably inhibited glioma cell proliferation, migration and invasion and promoted apoptosis and cell cycle arrest, while circRELN knockdown reversed these effects. MiR-1290 served as a target of circRELN, and glioma cell malignant phenotypes recovered by circRELN knockdown were partly repressed by miR-1290 deficiency. In addition, RORA was a target of miR-1290, and glioma cell malignant phenotypes promoted by miR-1290 restoration were partly blocked by RORA overexpression. CircRELN regulated RORA expression by targeting miR-1290. In Xenograft models, Sev inhibited tumor growth by upregulating circRELN. Conclusion Sev blocked the progression of glioma by increasing circRELN expression, and circRELN played roles in glioma partly by regulating the miR-1290/RORA network.

Abstract Background Gastrointestinal tumors are a leading cause of mortality worldwide. As shown in our previous study, miR-1290 is overexpressed in colorectal cancer (CRC) and promotes tumor progression. We therefore aimed to explore the potential of circulating miR-1290 as a biomarker for gastrointestinal cancer. Methods A serum miRNA sequencing analysis was performed. Then, circulating miRNA detection technologies were established. The expression of miR-1290 was analyzed in gastrointestinal tumor cell lines and culture supernatants. Expression levels of circulating miR-1290 in clinical samples were examined. Associations between miR-1290 expression and clinicopathologic characteristics were analyzed. Xenograft models were generated to assess the fluctuation in serum miR-1290 levels during disease progression. Results Through miRNA sequencing, we identified that miR-1290 was overexpressed in serum samples from patients with CRC. We confirmed that human gastrointestinal tumor cells express and secrete miR-1290. The circulating miR-1290 levels was up-regulated in patients with pancreatic cancer (PC) (p

Since circCDR1 was abnormally expressed in esophageal squamous cell cancer (ESCC), the current study explored whether circCDR1 affected ESCC. Detailedly, circCDR1 expression in ESCC and linear isoform and stability of circCDR1 were detected by RT-qPCR. The location of circCDR1 was detected by fluorescence in situ hybridization (FISH). After transfection, the cell biological functions were detected by wound-healing, CCK-8, colony formation, and flow cytometry assays. The target of circCDR1 was predicted by bioinformatics, FISH, RNA pull-down, and dual-luciferase reporter assays. The correlation between circCDR1 and miR-1290 was analyzed by Pearson's correlation analysis. A subcutaneous-xenotransplant tumor model in BALB/c nude mice was established and the levels of circCDR1, miR-1290, and apoptosis/metastasis/proliferation-related factors in the cancer cells and tissues were detected by immunohistochemical analysis, western blot, or RT-qPCR. As a result, circCDR1 was low-expressed in ESCC tissues and cells, while miR-1290 was high-expressed. CircCDR1 was regulated and was negatively correlated with miR-1290. CircCDR1, located in cytoplasm, inhibited the viability, proliferation, migration, and invasion of the cancer cells and the expressions of Bcl-2, N-cadherin, and Vimentin, but enhanced cell apoptosis and the expressions of C caspase-3, Bax, E-cadherin, IGFBP4, LHX6 and NFIX. In vivo, circCDR1 promoted xenotransplanted tumor weight and volume, and the expressions of C caspase-3 and Bax yet suppressed the levels of Bcl-2, miR-1290, and Ki-67 in tumor tissues. The effects of circCDR1 on both cancer cells and tissues were opposite to and reversed by miR-1290 mimic. Collectively, circCDR1 sponged miR-1290 to regulate the progression of ESCC both in vitro and in vivo. [ABSTRACT FROM AUTHOR]

Background: Circular RNAs (circRNAs) can function as competing endogenous RNAs (ceRNAs) to impact the development of esophageal squamous cell cancer (ESCC). Human circ_0001946 has been identified as a potential anticancer factor in ESCC, yet our understanding of its molecular basis remains limited. Methods: Circ_0001946, microRNA (miR)‐1290 and SRY‐box transcription factor 6 (SOX6) were quantified by quantitative reasl‐time PCR (qRT‐PCR) or immunoblotting. Cell proliferation was assessed by CCK‐8 and EDU assays. Cell apoptosis and invasion were evaluated by flow cytometry and transwell assays, respectively. Cell migration was detected by transwell and wound‐healing assays. The direct relationship between miR‐1290 and circ_0001946 or SOX6 was determined by dual‐luciferase reporter and RNA immunoprecipitation (RIP) assays. Xenograft model assays were used to assess the role of circ_0001946 in tumor growth. Results: Circ_0001946 expression was attenuated in human ESCC, and circ_0001946 increase impeded cell proliferation, invasion, migration and enhanced apoptosis in vitro. Moreover, circ_0001946 increase diminished xenograft growth in vivo. Mechanistically, circ_0001946 bound to miR‐1290, and re‐expression of miR‐1290 reversed circ_0001946‐dependent cell properties. SOX6 was a miR‐1290 target and it was responsible for the regulation of miR‐1290 in cell properties. Furthermore, circ_0001946 functioned as a ceRNA to regulate SOX6 expression via miR‐1290. Conclusion: Our findings uncover an undescribed molecular mechanism, the circ_0001946/miR‐1290/SOX6 ceRNA crosstalk, for the anti‐ESCC activity of circ_0001946. [ABSTRACT FROM AUTHOR]

To investigate the expression of microRNA (miR)-1290 and mir-1307 in plasma exosomes of patients with ovarian cancer, and to analyze their relationship with clinicopathological parameters and diagnostic value. 60 patients with ovarian cancer who were diagnosed and treated in Jingjiang People's Hospital from January 2019 to January 2021 were selected as the ovarian cancer group, 50 female health examiners during the same period as the healthy control group and 52 patients with benign ovarian tumors as the benign tumor group. Real-time quantitative PCR (qRT-PCR) was used to detect the expression of miR-1290 and miR-1307 in plasma exosomes of each group. The relationship between miR-1290, miR-1307 and clinicopathological characteristics of patients with ovarian cancer were analyzed. The receiver operating characteristic curve(ROC)was used to analyze the diagnostic efficacy of plasma exosomes miR-1290 and miR-1307 for ovarian cancer. Compared with benign ovarian tumor group and healthy control group, the expression of plasma exosomes miR-1290 and miR-1307 in ovarian cancer group were higher (P＜0.05). The expression of miR-1290 in the ovarian cancer group was related to the FIGO stage, degree of differentiation and lymph node metastasis, and the level of miR-1307 was related to the FIGO stage and lymph node metastasis (P＜0.05). There was a significant positive correlation between the expression of plasma exosomes miR-1307 and miR-1290 of patients with ovarian cancer (r＝0.478, P＜0.05). The area under curve (AUC) (0.95CI) of plasma exosomes miR-1290, miR-1307 and combined application in the diagnosis of ovarian cancer were 0.726 (0.526 ~ 0.926), 0.724 (0.466 ~ 0.987) and 0.845 (0.750 ~ 0.933), respectively. The diagnostic efficiency of combined application was higher than that of single application. The expression levels of plasma exosomes miR-1290 and miR-1307 in patients with ovarian cancer are increased. The combined detection of miR-1290 and miR-1307 has high value in the early diagnosis of ovarian cancer, and is expected to become a new molecular marker of ovarian cancer. [ABSTRACT FROM AUTHOR]

Abstract Background Sarcopenia is a common skeletal disease related to myogenic disorders and muscle atrophy. Current clinical management has limited effectiveness. We sought to investigate the role of miR-1290 in myoblast differentiation and muscle atrophy. Methods By transfecting miR-1290 into C2C12 cells, we investigated whether miR-1290 regulates myogenesis and myotube atrophy via AKT/P70 signaling pathway. MHC staining was performed to assess myoblast differentiation. Differentiation-related MHC, Myod, and Myog protein levels, and atrophy-related MuRF1 and atrogin-1 were explored by western blot. An LPS-induced muscle atrophy rat model was developed. RT-PCR was conducted to analyze miR-1290 serum levels in muscle atrophy patients and normal controls (NCs). Results The miR-1290 transfection increased MHC-positive cells and MHC, Myod, and Myog protein levels in the miR-1290 transfection group, demonstrating that miR-1290 promoted C2C12 myoblast differentiation. Myotube diameter in the miR-1290 transfection group was higher than in the TNF-α-induced model group. Western blot analysis showed decreased MuRF1 and atrogin-1 levels in the miR-1290 transfection group compared with the model group, demonstrating that miR-1290 protected against myoblast cellular atrophy. Luciferase assay and western blot analysis showed that miR-1290 regulation was likely caused by AKT/p70/FOXO3 phosphorylation activation. In the LPS-induced muscle atrophy rat model, miR-1290 mimics ameliorated gastrocnemius muscle loss and increased muscle fiber cross-sectional area. Clinically, miR-1290 serum level was significantly decreased in muscle atrophy patients. Conclusions We found that miR-1290 enhances myoblast differentiation and inhibits myotube atrophy through Akt/p70/FoxO3 signaling in vitro and in vivo. In addition, miR-1290 may be a potential therapeutic target for sarcopenia treatment.

Background: MicroRNA-1290 (miR-1290) has been reported to be involved in many diseases and play a key role during the development process. However, the role of miR-1290 in atherosclerosis (AS) is still unclear. Methods and results: The current study showed that the expressions of miR-1290 were high in serum of patients with hyperlipidemia. The functional role of miR-1290 were then investigated in human umbilical vein endothelial cells (HUVECs). Here, we found that miR-1290 expressions were notably enhanced in HUVECs mediated by IL-8. miR-1290 inhibitor repressed monocytic THP-1 cells adhesion to HUVECs by regulating ICAM-1 and VCAM-1, inhibited proliferation through regulating cyclinD1 and PCNA, and inhibited inflammatory response by regulating IL-1β. Mechanistically, we verified that miR-1290 mimic was able to directly target the 3′-UTR of GSK-3β mRNA using luciferase reporter assay. Knockdown of GSK-3β (si-GSK-3β) promoted HUVECs adhesion and the expression of IL-1β, and partially restore the depression effect of miR-1290 inhibitor on HUVECs adhesion and inflammation. In contrast, si-GSK-3β inhibited the proliferation of HUVECs and the expression of cyclinD1 and PCNA. Conclusions: In summary, our study revealed that miR-1290 promotes IL-8-mediated the adhesion of HUVECs by targeting GSK-3β. However, GSK-3β is not the target protein for miR-1290 to regulate the proliferation of HUVECs. Our findings may provide potential target in atherosclerosis treatment. [ABSTRACT FROM AUTHOR]

Abstract Background Circular RNA (circRNA), an novel type of non-coding RNA, could interact with miRNA and protein molecules to regulate the occurrence and progression of hepatocellular carcinoma (HCC). However, little is known about the pathogenesis of circ_0004913 in HCC. Materials Through the GEO (Gene Expression Omnibus database) to find dysfunctional circRNAs in HCC, and circ_0004913 was selected as the research object. Quantitative reverse transcription PCR (qRT-PCR) was used to detect the expression level of circ_0067934 in HCC tissues and cells. CCK-8, Edu and flow cytometry assays were used to determine the malignant behavior of transfected HCC cells. Mechanistically, RNA immunoprecipitation and dual-luciferase reporter gene assay were performed to explore the relation between circ_0067934, miR-1290 and FOXC1 (Forkhead box C1) in HCC. Results The expression of circ_0004913 was down-regulated in HCC tissues and cell lines, while the overexpression of circ_0004913 attenuates the malignant behavior of HCC cells. Bioinformatics predicted that circ_0004913 interacts with miR-1290, which targeted FOXC1 mRNA. In fact, miR-1290 promoted the malignant behavior of HCC cells, while FOXC1 had the opposite effect. In addition, circ_0004913 overexpression enhanced FOXC1 expression by reducing miR-1290 expression, thereby inhibiting the proliferation of HCC cells. Conclusions Circ_0004913 / miR-1290 / FOXC1 regulatory axis could inhibit the progress of HCC. Our findings may provide potential new targets for the diagnosis and treatment of HCC.

MicroRNAs (miRNAs) have been shown to affect expression of several genes contributing in important biological processes. miR-1290 a member of this family with crucial roles in the carcinogenesis. This miRNA is transcribed from MIR1290 gene on chromosome 1p36.13. This miRNA has interactions with a number of mRNA coding genes as well as non-coding RNAs SOCS4, GSK3, BCL2, CCNG2, KIF13B, INPP4B, hMSH2, KIF13B, NKD1, FOXA1, IGFBP3, CCAT1, FOXA1, NAT1, SMEK1, SCAI, ZNF667-AS1, ABLIM1, Circ_0000629 and CDC73. miR-1290 can also regulate activity of JAK/STAT3, PI3K/AKT, Wnt/β-catenin and NF-κB molecular pathways. Most evidence indicates the oncogenic roles of miR-1290, yet controversial evidence also exists. In the present review, we describe the results of in vitro, animal and human investigations about the impact of miR-1290 in the development of malignancies.

Background: Sevoflurane (Sev) has been reported to inhibit cancer development, and sevoflurane treatment in cancers is implicated with the deregulation of specific non-coding RNAs (ncRNAs). This study aimed to investigate the relationship between sevoflurane and circular RNA reelin (circRELN) in glioma. Methods: The expression of circRELN, microRNA-1290 (miR-1290) and RAR-related orphan receptor A (RORA) was measured by quantitative real-time PCR (qPCR). Cell proliferative capacity was assessed by cell counting kit-8 (CCK-8) and colony formation assays. Cell apoptosis and cell cycle distribution were monitored by flow cytometry assay. Cell migration was assessed by wound healing assay and transwell assay, and cell invasion was assessed by transwell assay. The protein levels of matrix metalloproteinase-2 (MMP2), MMP9 and RORA were quantified by western blot. Tumor growth in vivo was assessed by Xenograft models. The binding relationship between miR-1290 and circRELN or RORA was verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Results: We found that circRELN expression was declined in glioma tissues and cells, while Sev treatment enhanced circRELN expression. In function, Sev notably inhibited glioma cell proliferation, migration and invasion and promoted apoptosis and cell cycle arrest, while circRELN knockdown reversed these effects. MiR-1290 served as a target of circRELN, and glioma cell malignant phenotypes recovered by circRELN knockdown were partly repressed by miR-1290 deficiency. In addition, RORA was a target of miR-1290, and glioma cell malignant phenotypes promoted by miR-1290 restoration were partly blocked by RORA overexpression. CircRELN regulated RORA expression by targeting miR-1290. In Xenograft models, Sev inhibited tumor growth by upregulating circRELN. Conclusion: Sev blocked the progression of glioma by increasing circRELN expression, and circRELN played roles in glioma partly by regulating the miR-1290/RORA network. [ABSTRACT FROM AUTHOR]

Background: Gastrointestinal tumors are a leading cause of mortality worldwide. As shown in our previous study, miR-1290 is overexpressed in colorectal cancer (CRC) and promotes tumor progression. We therefore aimed to explore the potential of circulating miR-1290 as a biomarker for gastrointestinal cancer.Methods: A serum miRNA sequencing analysis was performed. Then, circulating miRNA detection technologies were established. The expression of miR-1290 was analyzed in gastrointestinal tumor cell lines and culture supernatants. Expression levels of circulating miR-1290 in clinical samples were examined. Associations between miR-1290 expression and clinicopathologic characteristics were analyzed. Xenograft models were generated to assess the fluctuation in serum miR-1290 levels during disease progression.Results: Through miRNA sequencing, we identified that miR-1290 was overexpressed in serum samples from patients with CRC. We confirmed that human gastrointestinal tumor cells express and secrete miR-1290. The circulating miR-1290 levels was up-regulated in patients with pancreatic cancer (PC) (p < 0.01), CRC (p < 0.05), and gastric cancer (GC) (p < 0.01). High miR-1290 expression levels were associated with tumor size, lymphatic invasion, vascular invasion, distant metastasis, tumor differentiation and AJCC stage in patients with PC and CRC. The area under the curve (AUC) was 0.8857 in patients with PC, with 60.9% sensitivity and 90.0% specificity. The AUC was 0.7852 in patients with CRC, with 42.0% sensitivity and 90.0% specificity. In patients with GC, the AUC was 0.6576, with 26.0% sensitivity and 90.0% specificity. The in vivo model verified that the circulating miR-1290 level was significantly increased after tumor formation and decreased after drug treatment.Conclusions: Our findings indicate that circulating miR-1290 is a potential biomarker for gastrointestinal cancer diagnosis and monitoring. [ABSTRACT FROM AUTHOR]

Myocardial infarction (MI) remains a leading cause of morbidity and mortality worldwide. Endothelial progenitor cell (EPC)-derived exosomes have been found to be effective in alleviating MI, while the detailed mechanisms remain unclear. The present study aimed to determine the protective effects of EPC-derived exosomal miR-1246 and miR-1290 on MI-induced injury and to explore the underlying molecular mechanisms. The exosomes were extracted from EPCs; gene expression levels were determined by quantitative real-time PCR, and protein expression levels were determined by western blot and immunofluorescence staining, respectively. The angiogenesis and proliferation of human cardiac fibroblasts (HCFs) were determined by tube formation assay and immunofluorescence staining of PKH67, respectively. Luciferase reporter, CHIP, and EMSA assays determined the interaction between miR-1246/1290 and the targeted genes (EFL5 and SP1). The protective effects of miR-1246/1290 on MI were evaluated in a rat model of MI. EPC-derived exosomes significantly upregulated miR-1246 and miR-1290 expression and promoted phenotypic changes of fibroblasts to endothelial cells, angiogenesis, and proliferation in HCFs. Exosomes from EPCs with miR-1246 or miR-1290 mimics transfection promoted phenotypic changes of fibroblasts to endothelial cells and angiogenesis in HCFs, while exosomes from EPCs with miR-1246 or miR-1290 knockdown showed opposite effects in HCFs. Mechanistically, miR-1246 and miR-1290 from EPC-derived exosomes induced upregulation of ELF5 and SP1, respectively, by targeting the promoter regions of corresponding genes. Overexpression of both ELF5 and SP1 enhanced phenotypic changes of fibroblasts to endothelial cells and angiogenesis in HCFs pretreated with exosomes from EPCs with miR-1246 or miR-1290 mimics transfection, while knockdown of both EFL5 and SP1 exerted the opposite effects in HCFs. Both ELF5 and SP1 can bind to the promoter of CD31, leading to the upregulation of CD31 in HCFs. Furthermore, in vivo animal studies showed that exosomes from EPCs with miR-1246 or miR-1290 overexpression attenuated the MI-induced cardiac injury in the rats and caused an increase in ELF5, SP1, and CD31 expression, respectively, but suppressed α-SMA expression in the cardiac tissues. In conclusion, our study revealed that miR-1246 and miR-1290 in EPC-derived exosomes enhanced in vitro and in vivo angiogenesis in MI, and these improvements may be associated with amelioration of cardiac injury and cardiac fibrosis after MI.

Dysregulated circular RNAs (circRNAs) have been confirmed to partake in the modulation of the glioma progression. Here, we intended to explore the role of circBRAF in glioma and the possible action mechanism. The expression levels of circBRAF, microRNA (miR)-1290 and F-box and WD repeat domain containing 7 (FBXW7) were analyzed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) or western blot. Cell viability was assessed by 3-(4, 5)-dimethylthiazole-2-y1)-2, 5-biphenyl tetrazolium bromide (MTT) assay. Cell cycle distribution was determined by flow cytometry. Cell migration and invasion were evaluated through Trans-well assay. Related protein levels were detected by western blot. Targeted relation among circBRAF, miR-1290 and FBXW7 was validated by dual-luciferase reporter, RNA immunoprecipitation (RIP) and pull-down assays. Xenograft model was constructed to explore the function of circBRAF in vivo. Expression of circBRAF and FBXW7 was decreased in glioma tissues and cells. Upregulation of circBRAF inhibited glioma cell proliferation and metastasis in vitro. MiR-1290 was upregulated in glioma, which was sponged by circBRAF. Besides, circBRAF elevated FBXW7 expression by targeting miR-1290. Introduction of miR-1290 or FBXW7 knockdown could counteract the inhibitory effects of circBRAF upregulation on the malignant phenotypes of glioma cells. Overexpression of circBRAF repressed the tumor growth in vivo. Upregulation of circBRAF suppressed glioma evolvement in vitro and in vivo by regulating miR-1290/FBXW7 axis, broadening the cognition of glioma progression. [ABSTRACT FROM AUTHOR]

Background: Sarcopenia is a common skeletal disease related to myogenic disorders and muscle atrophy. Current clinical management has limited effectiveness. We sought to investigate the role of miR-1290 in myoblast differentiation and muscle atrophy. Methods: By transfecting miR-1290 into C2C12 cells, we investigated whether miR-1290 regulates myogenesis and myotube atrophy via AKT/P70 signaling pathway. MHC staining was performed to assess myoblast differentiation. Differentiation-related MHC, Myod, and Myog protein levels, and atrophy-related MuRF1 and atrogin-1 were explored by western blot. An LPS-induced muscle atrophy rat model was developed. RT-PCR was conducted to analyze miR-1290 serum levels in muscle atrophy patients and normal controls (NCs). Results: The miR-1290 transfection increased MHC-positive cells and MHC, Myod, and Myog protein levels in the miR-1290 transfection group, demonstrating that miR-1290 promoted C2C12 myoblast differentiation. Myotube diameter in the miR-1290 transfection group was higher than in the TNF-α-induced model group. Western blot analysis showed decreased MuRF1 and atrogin-1 levels in the miR-1290 transfection group compared with the model group, demonstrating that miR-1290 protected against myoblast cellular atrophy. Luciferase assay and western blot analysis showed that miR-1290 regulation was likely caused by AKT/p70/FOXO3 phosphorylation activation. In the LPS-induced muscle atrophy rat model, miR-1290 mimics ameliorated gastrocnemius muscle loss and increased muscle fiber cross-sectional area. Clinically, miR-1290 serum level was significantly decreased in muscle atrophy patients. Conclusions: We found that miR-1290 enhances myoblast differentiation and inhibits myotube atrophy through Akt/p70/FoxO3 signaling in vitro and in vivo. In addition, miR-1290 may be a potential therapeutic target for sarcopenia treatment. [ABSTRACT FROM AUTHOR]

Background: MicroRNAs (miRNAs) are small noncoding RNAs (containing approximately 22 nucleotides), which modulate and control the expression of target genes by binding them. MiRNAs play a crucial role in tumorigenesis. Thus, alterations in the expression level of miRNAs play a key role in the pathobiology of numerous cancers. In this research, the expression level of MicroRNA-1290 (miR1290) and its target genes THBS1 and DKK3 were evaluated in colorectal cancer (CRC) patients. Methods: This case-control study was carried out on 144 paraffin-embedded tissue samples of CRC and adjacent tissues from patients who referred to Imam Khomeini Hospital, Tehran, Iran. Total RNA was isolated from the tissue using Trizol reagent following the manufacturer’s instructions and then reverse transcribed to cDNA. The expression of miR-1290 and its target genes was measured by quantitative Real-Time PCR (qRT-PCR). Statistical analyses were performed using SPSS V.20 statistical software. Results: We present evidence that the miR-1290 expression in CRC tissues was significantly higher than in the normal margin, and its targets were downregulated in tumor tissue compared to the adjacent tissue. Conclusion: This study supports the essential role of miR-1290 and its contribution to CRC invasion and metastasis through targeting THBS1 and DKK3, as biomarkers for CRC diagnosis.

Abstract Background microRNAs (miRNAs) stably exist in circulating blood encapsulated in extracellular vesicles such as exosomes; therefore, serum miRNAs have the potential to serve as novel cancer biomarkers. New diagnostic markers to detect high grade serous ovarian cancer (HGSOC) are urgently needed. The aim of this study was to identify miRNAs specific to HGSOC and analyze whether serum miRNA can discriminate HGSOC patients from healthy controls or patients with ovarian malignancies of other histological types. Methods Exosomes from ovarian cancer cell lines were collected and exosomal miRNAs extracted. miRNA microarray analysis revealed several elevated miRNAs specific to HGSOC. Among these, we focused on miR-1290. Sera from 70 ovarian cancer patients and 13 healthy controls were gathered and its expression levels detected by quantitative real-time polymerase chain reaction. Results In HGSOC patients, serum miR-1290 was significantly overexpressed compared to in healthy controls (3.52 fold; P = 0.03), unlike in patients with ovarian cancers of other histological types. The relative expression of miR-1290 was higher in advanced stages of HGSOC than in early stages (4.23 vs. 1.58; P = 0.23). Its expression significantly decreased after operation (5.87 to 1.17; P

Altered expression of microRNAs (miRNAs) is implicated in fetal growth. However, the mechanisms by which placenta-derived miRNAs regulate birthweight are not well understood. In Phase 1, we compared the expression of 754 miRNAs in the placenta from two extreme birthweight groups (0.8–2.2 kg vs. 3.3–3.9 kg, n = 77 each) selected from an arsenic-exposed Bangladeshi birth cohort (n = 1,141). We identified 49 miRNAs associated with the extreme birthweight groups and/or gestational age in Phase 1, which were further analyzed in Phase 2 among 364 randomly selected mother-infant pairs. Gestational age was determined by ultrasound. Causal mediation analysis was used to estimate the effect of miRNAs on birthweight considering gestational age a mediator, adjusting for cord blood arsenic and other risk factors. miR-1290, miR-195, and let-7g showed significant inverse associations with gestational age, while miR-328 showed significant positive association [false discovery rate (FDR)

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Background: MicroRNAs (miRNAs) are small noncoding RNAs (containing approximately 22 nucleotides), which modulate and control the expression of target genes by binding them. MiRNAs play a crucial role in tumorigenesis. Thus, alterations in the expression level of miRNAs play a key role in the pathobiology of numerous cancers. In this research, the expression level of MicroRNA-1290 (miR- 1290) and its target genes THBS1 and DKK3 were evaluated in colorectal cancer (CRC) patients. Methods: This case-control study was carried out on 144 paraffin-embedded tissue samples of CRC and adjacent tissues from patients who referred to Imam Khomeini Hospital, Tehran, Iran. Total RNA was isolated from the tissue using Trizol reagent following the manufacturer's instructions and then reverse transcribed to cDNA. The expression of miR-1290 and its target genes was measured by quantitative Real- Time PCR (qRT-PCR). Statistical analyses were performed using SPSS V.20 statistical software. Results: We present evidence that the miR-1290 expression in CRC tissues was significantly higher than in the normal margin, and its targets were downregulated in tumor tissue compared to the adjacent tissue. Conclusion: This study supports the essential role of miR-1290 and its contribution to CRC invasion and metastasis through targeting THBS1 and DKK3, as biomarkers for CRC diagnosis. [ABSTRACT FROM AUTHOR]

MAF is a transcription factor that may act either as a tumor suppressor or as an oncogene, depending on cell type. We have shown previously that the overexpressed miR-1290 influences MAF protein levels in LSCC (laryngeal squamous cell carcinoma) cell lines. In this study, we shed further light on the interaction between miR-1290 and MAF, as well as on cellular MAF protein localization in LSCC. We confirmed the direct interaction between miR-1290 and MAF 3′UTR by a dual-luciferase reporter assay. In addition, we used immunohistochemistry staining to analyze MAF protein distribution and observed loss of MAF nuclear expression in 58% LSCC samples, of which 10% showed complete absence of MAF, compared to nuclear and cytoplasmatic expression in 100% normal mucosa. Using TCGA data, bisulfite pyrosequencing and CNV analysis, we excluded the possibility that loss-of-function mutations, promoter region DNA methylation or CNV are responsible for MAF loss in LSCC. Finally, we identified genes involved in the regulation of apoptosis harboring the MAF binding motif in their promoter region by applied FIMO and DAVID GO analysis. Our results highlight the role of miR-1290 in suppressing MAF expression in LSCC. Furthermore, MAF loss or mislocalization in FFPE LSCC tumor samples might suggest that MAF acts as a LSCC tumor suppressor by regulating apoptosis.

5-Fluorouracil (5FU)-based adjuvant therapy is the first-line therapy for treating stage II and III colon cancer after surgery. However, its therapeutic efficacy is limited because of chemoresistance, especially in deficient mismatch repair (dMMR) colon cancer. Here, we first used laser capture microdissection to obtain purified cells from four dMMR and four proficient mismatch repair (pMMR) colon cancer tissues. Second, microRNA (miRNA) microarray chips were used to identify miRNAs that are differentially expressed between these two classes of tumors. Third, we analyzed their differential expression by qRT-PCR in a panel of 5-FU-resistant colon cancer cell lines. We identified that miR-1290 was one of the most upregulated miRNAs in both dMMR colon cancer tissues and 5-FU-resistant cells. We also found that miR-1290 was positively correlated with dMMR status and predicted poor prognosis in stage II and III colon cancer patients who received 5-FU-based chemotherapy. Furthermore, we demonstrated that inhibition of the expression of miR-1290 enhanced sensitivity to 5-FU treatment in vitro and in tumor xenografts in vivo by direct targeting hMSH2. Our study indicates that miR-1290 may become a promising biomarker of dMMR colon cancer and predicts the prognosis of stage II and III patients who receive 5-FU-based adjuvant therapy.

Background & Objective: This study aimed to determine the incidence of microRNA (miRNA; miR-1290) in the serum of oral squamous cell carcinoma (OSCC) patients compared to a control group using the qualitative real-time polymerase chain reaction (PCR) method., Methods: Blood serum samples were obtained from patients diagnosed with OSCC and confirmed through biopsy. The samples were collected from patients referred to the Mashhad Dental Faculty and Ghaem Hospital. The OSCC group consisted of 17 patients, while the healthy group included 15 individuals. RNA was extracted from the patient samples, and samples with an A260/280 ratio between 1.8 and 2.0 (indicating acceptable RNA quality) were immediately converted into complementary DNA (cDNA) using albumin and cDNA reference genes. The SYBR green real-time reverse transcriptase PCR method was used to measure the presence of miR-1290 in the blood samples., Results: A total of 32 patients were examined in this study, including 17 women (53.1%) and 15 men (46.9%). The mean age was 46.7 years in the healthy group and 54.6 years in the SCC group, indicating a significant difference ( P <0.05). The expression level of the miR-1290 gene was higher in patients with SCC compared to the healthy group ( P =0.000). While the expression level of miR-1290 was higher in grade 3 and advanced stage than in grades 2 and 1 and early stage, the differences were not statistically significant ( P =0.173 and P =0.564 for grade and stage, respectively)., Conclusion: The expression level of miR-1290 may increase in SCC patients compared to healthy individuals, making it a potential circulating biomarker. Further investigations for diagnostic utility would be warranted., Competing Interests: The authors declare no conflict of interest., (© 2024.)

OBJECTIVE: MicroRNAs (miRNAs) have been demonstrated to be involved in the pathogenesis of various human cancers, including oral squamous cell carcinoma (OSCC). Here, we designed this study to explore the potential effect of miR-1290 on tumorigenesis of OSCC. PATIENTS AND METHODS: The expressions of miR-1290 and cyclin G2 (CCNG2) in OSCC were observed by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Dual-Luciferase Reporter Assay was performed to confirm the relationship between miR-1290 and CCNG2. The functions of miR- 1290 and CCNG2 were analyzed using transwell assay. The Western blot analysis was used to detect epithelial-mesenchymal transition (EMT). RESULTS: Upregulation of miR-1290 and downregulation of CCNG2 were identified in OSCC. And upregulation of miR-1290 was associated with clinicopathological characteristics and poor prognosis in OSCC patients. Moreover, the downregulation of miR-1290 inhibited cell metastasis and EMT in OSCC cells. Furthermore, CCNG2 was a direct target of miR-1290. Its expression was inversely regulated by miR-1290 in OSCC cells. At the same time, the suppressive effect of CCNG2 was observed in OSCC. Furthermore, overexpression of CCNG2 weakened the promoted effect of miR-1290 on cell metastasis in OSCC. CONCLUSIONS: MiR-1290 promoted cell metastasis and EMT, inhibiting CCNG2 expression in OSCC. [ABSTRACT FROM AUTHOR]

Background: Enhancing the diagnostic efficacy of early-stage lung cancer is crucial for improving prognosis. The objective of this study was to ascertain dependable exosomal miRNAs as biomarkers for the diagnosis of lung cancer., Methods: Exosomal miRNA candidates were identified through miRNA sequencing and subsequently validated in various case-control sets using real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR). The correlation between the expression of exosomal miRNAs and the clinicopathological features of lung cancer was investigated. To assess the diagnostic efficacy of exosomal miRNAs for lung cancer, the receiver operating characteristic (ROC) curve analysis was conducted. The optimal cutoff value of exosomal miRNAs was determined in the testing cohort and subsequently confirmed in the validation cohort., Results: The results showed that the expression of exosomal miR-1290 was significantly elevated, while that of miR-29c-3p was significantly decreased in the plasma of lung cancer patients, especially in those with early-stage lung cancer, compared to individuals with benign lung conditions (P < 0.01). Exosomal miR-1290 and miR-29c-3p demonstrated superior diagnostic efficacy compared to conventional tumor biomarkers in distinguishing between lung cancer and benign lung diseases, as evidenced by their respective area under the curve (AUC) values of 0.934 and 0.868. Furthermore, exosomal miR-1290 and miR-29c-3p exhibited higher diagnostic efficiency in early-stage lung cancer than traditional tumor markers, with AUC values of 0.947 and 0.895, respectively. Notably, both exosomal miR-1290 and miR-29c-3p displayed substantial discriminatory capacity in distinguishing between non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC), as indicated by their respective AUC values of 0.810 and 0.842., Conclusions: The findings of this study provided evidence that exosomal miR-1290 and miR-29c-3p hold significant potential as biomarkers for the early detection of lung cancer, as well as for differentiating between NSCLC and SCLC., Competing Interests: 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., (© 2023 The Authors.)

To investigate the interaction of miR‐1290 and LHX6 in gliomas, and their influence on the propagation and metastasis of glioma cells. The differential expression of miR‐1290 in glioma cells was identified by chip screening. The expression level of miR‐1290 and LHX6 were determined by qRT‐PCR and Western blot. The influence of miR‐1290 on propagation of glioma cells were analyzed by MTT assay, EdU incorporation, and colony formation, while the impact of miR‐1290 on metastasis was assessed by transwell assay. The relationship between LHX6 and miR‐1290 was testified by luciferase reporter assay. The gliomas orthotopic implantation model of nude mice was established to investigate the influence of miR‐1290 and LHX6 on tumor growth. Tumor volumes were evaluated by photon density, and the expression of Ki67 protein was analyzed by immunohistochemistry. MiR‐1290 presented a higher expression in glioma cells and tissues. MiR‐1290 overexpression significantly promoted propagation and metastasis of glioma cells, while miR‐1290 knockdown inhibited glioma development. MiR‐1290 suppressed LHX6 expression, facilitating development of glioma cells. The orthotopic implantation model showed that miR‐1290 overexpression promoted tumor growth while LHX6 overexpression inhibited it. MiR‐1290 could promote glioma cell propagation and metastasis by inhibiting LHX6. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) is one of the most common oncological conditions worldwide, to date. MicroRNA- 1290 (miR-1290) has been demonstrated to regulate its progression. We studied the role of miR-1290 in CRC progression. The gene was upregulated in CRC tissues and cells. Its overexpression promoted CRC cell proliferation analyzed by MTT assay, colony formation assay, and soft agar growth assay. In addition, miR-1290 knockdown inhibited CRC cell proliferation. We also found that miR-1290 overexpression reduced the p27 level and increased cyclin D1 at both the mRNA and protein levels, whereas miR-1290 knockdown increased p27 and reduced cyclin D1, confirming miR-1290 promoted CRC cell proliferation. Inositol polyphosphate 4-phosphatase B (INPP4B) was the target of miR-1290. Luciferase reporter assay revealed that miR-1290 directly bound to the 3¢-UTR of INPP4B; the mutated seed sites in miR-1290 abrogated this effect. Double knockdown of INPP4B and miR-1290 promoted CRC cell proliferation, suggesting miR-1290 promoted CRC cell proliferation by targeting INPP4B. [ABSTRACT FROM AUTHOR]

Altered expression of microRNAs (miRNAs) is implicated in fetal growth. However, the mechanisms by which placenta-derived miRNAs regulate birthweight are not well understood. In Phase 1, we compared the expression of 754 miRNAs in the placenta of mothers from two extreme birthweight groups (0.8-2.2 kg vs. 3.3-3.9 kg, n = 77 each) selected from an arsenic-exposed Bangladeshi birth cohort (n = 1,141). We identified 49 miRNAs associated with the extreme birthweight groups and/or gestational age in Phase 1, which were further analyzed in Phase 2 among 364 randomly selected mother-infant pairs. Gestational age was determined by ultrasound. Causal mediation analysis was used to estimate the effect of miRNAs on birthweight considering gestational age a mediator, adjusting for core blood arsenic and other risk factors. miR-1290, miR-195, and let-7g showed significant inverse associations with gestational age, while miR-328 showed significant positive association [false discovery rate (FDR) <0.05]. Via changing gestational age, miR-1290, miR-195, and miR-27a showed significant inverse associations with birthweight, while miR-328 and miR-324-5p showed significant positive associations (FDR <0.05). The effect of miRNAs on birthweight varied by gestational age (for miR-1290, miR-195, miR-328) and in utero arsenic exposure (for miR-1290): stronger effect was observed among infants delivered early in gestation or exposed to higher concentrations of arsenic in cord blood. Gene enrichment analysis with in silico predicted targets identified cell proliferation, inflammation, apoptosis, insulin, and IGF family signaling cascades associated with these miRNAs. Future studies are warranted to replicate these findings and assess these miRNAs as early biomarkers of fetal growth. [ABSTRACT FROM AUTHOR]

MicroRNAs are small endogenous non-coding RNAs, which can frequently emerge as regulators in many cancer types. MiR-1290 was found to be abnormally elevated in non small cell lung cancer (NSCLC). However, the underlying molecular mechanism still needs to be investigated. Here, we demonstrated that miR-1290 expression levels were remarkably upregulated in NSCLC tissues compared to adjacent normal tissues. Higher miR-1290 expression levels positively associated with lymph node metastasis and advanced tumor stage. Functional assays showed that upregulated miR-1290 expression in NSCLC cells enhanced cell proliferation, cell colony formation and invasion capacities in vitro. Furthermore, we found that miR-1290 promoted cell proliferation related protein CDK2 and CDK4 expression and enhanced Epithelial-Mesenchymal Transition (EMT) process by downregulating E-cadherin expression and upregulating N-cadherin expression. Bioinformatics analysis and luciferase reporter gene assays revealed that Interferon regulatory factor 2 (IRF2) was a direct target of miR-1290. Overexpression of miR-1290 can degrade IRF2 mRNA and downregulated IRF2 protein expression in NSCLC cells. Upregulated IRF2 could partly rescue the promoting effects induced by miR-1290 overexpression on cell proliferation and invasion of NSCLC. Additionally, we confirmed that reduced miR-1290 expression could suppress tumor growth using a tumor xenograft model in vivo. Thus, we concluded that miR-1290 may serve as a potential target of NSCLC treatment. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Ovarian cancer is one of the leading causes of cancer-related death in women, but treatment remained unsatisfactory. Studies have shown that lncRNA colon cancer-associated transcript 1 (CCAT1) plays an important regulatory role in different cancers, but its role in ovarian cancer remained largely unclear. PATIENTS AND METHODS: Quantitative Real-time polymerase chain reaction (qRT-PCR) was applied to detect the expression of lncRNA CCAT1 in ovarian cancer and adjacent tissue, and analysis was applied to explore the relationship between expression and clinical characteristic. After lncRNA CCAT1 suppression, Cell Counting Kit-8 (CCK8) and wound-healing assay were used to detect the proliferation and metastasis ability of ovarian cancer, respectively. RESULTS: qRT-PCR showed that lncRNA CCAT1 was highly expressed in ovarian cancer tissue, compared with adjacent tissue. Moreover, we found that the expression of lncRNA CCAT1 was closely related to prognosis, tumor size, and lymph node metastasis. We also found that lncRNA CCAT1 could sponge miR-1290 in ovarian cancer. CONCLUSIONS: In this study, we found that lncRNA CCAT1 could sponge miR-1290 in ovarian cancer, and was closely related to prognosis, proliferation, and metastasis. [ABSTRACT FROM AUTHOR]

Asiatic acid (AA) could attenuate ischemia/reperfusion induced myocardial apoptosis through upregulating the Akt/GSK-3β/HIF-1α pathway. HIF-3α is a negative regulator of HIF-1α, whose mRNA is a potential target of miR-1290. AA could upregulate miR-1290 in non-small-cell lung cancer A549 cells. This work aimed to investigate whether AA could inhibit hypoxia induced cardiomyocyte apoptosis through regulating the miR-1290/HIF3A/HIF-1α axis. The AC16 human myocardial cell line cultured under normoxic or hypoxic conditions was treated with various doses of AA for 24 h. Afterwards cell viability, apoptosis and the expression of miR-1290, HIF3A, and HIF1A were evaluated. Cells transfected with miR-1290 mimic or inhibitor were used to determine the role of miR-1290 in the anti-apoptosis effect of AA and the expression of HIF3A and HIF1A. Dual luciferase assay was performed to confirm miR-1290 targeting of HIF3A. HIF3A overexpression was achieved by transfection of HIF3A1 overexpressing lentivirus, and its effect on miR-1290 and AA-regulated survival of cardiomyocytes was evaluated. AA treatment protected cardiomyocytes from hypoxia-induced apoptosis and upregulated miR-1290 and HIF1A, but downregulated HIF3A under hypoxia. The protective effect of AA was abolished by miR-1290 knockdown, whereas enhanced by miR-1290 overexpression. In addition, miR-1290 knockdown increased HIF1A expression, but reduced HIF3A expression in cardiomyocytes. Dual luciferase assay confirmed miR-1290 direct targeting the 3′ UTR of HIF3A. HIF3A overexpression counteracted the anti-apoptosis effect of AA or miR-1290. In conclusion, AA can protect cardiomyocytes against hypoxia-induced apoptosis through regulating the miR-1290/HIF3A/HIF-1α axis, and miR-1290 may be a potential target in the prevention of myocardial ischemia-reperfusion injury. © 2017 IUBMB Life, 69(9):660-667, 2017 [ABSTRACT FROM AUTHOR]

Background: Circulating microRNAs (miRNAs) are attracting major interest as potential non-invasive biomarkers for colorectal cancer (CRC). This study aimed to identify a novel serum miRNA biomarker for the early detection and/or evaluating prognosis of CRC patients. Patients and methods: Comprehensive miRNA array analysis was carried out using serum samples from patients with colorectal neoplasia and healthy controls. Next, to verify whether the candidate miRNA possessed a secretory potential, we screened miRNA expression levels in culture medium from 2 CRC cell lines, followed by serum analysis from 12 stage IV CRC, 12 adenoma, and 12 control subjects. Thereafter, we validated expression of candidate miRNAs in 179 primary CRC tissues, as well as serum samples from an independent cohort of 211 CRCs, 56 adenomas, and 57 control subjects. Results: Through microarray analysis, we identified significantly higher levels of miRNA-1290 (miR-1290) in serum from patients with colorectal adenomas and cancers. We verified miR-1290 overexpression in serum of CRC patients in a training cohort. In the validation cohort, serum miR-1290 levels were significantly up-regulated in patients with colorectal adenomas (P < 0.0001) and cancers (P < 0.0001). Serum miR-1290 levels could robustly distinguish adenoma [area under the curve (AUC) = 0.718] and CRC patients (AUC = 0.830) from normal subjects. High miR-1290 expression in serum and tissue was significantly associated with tumor aggressiveness and poor prognosis. Moreover, serum miR-1290 levels were an independent prognostic factor [hazard ratio (HR) = 4.51; 95% confidence interval (CI) = 1.23-23.69; P=0.0096] and an independent predictor for tumor recurrence (hazard ratio = 3.92; 95% confidence interval = 1.11-25.14; P=0.032) inCRC. Conclusions: Serum miR-1290 is a novel biomarker for early detection, recurrence, and prognosis in CRC. [ABSTRACT FROM AUTHOR]

MicroRNA (miRNA) expression is altered in cancer cells and is associated with the development and progression of various types of cancer. Accordingly, miRNAs may serve as diagnostic or prognostic biomarkers in cancer patients. In this study, we attempted to analyze circulating exosomal miRNA in patients with cervical cancer. Total RNA was extracted from the serum of healthy subjects, subjects with cervical intraepithelial neoplasia (CIN) and patients with cervical cancer. We first investigated miRNA expression profiles in 6 serum samples from healthy subjects and patients with cervical cancer using the miRCURY LNA microRNA array. miRNAs with significant differences in expression were validated in a larger sample set by quantitative reverse transcription-polymerase chain reaction, using TaqMan gene expression assays. The results of the miRCURY LNA microRNA array indicated that 6 of 1,223 miRNAs found in serum samples from cervical cancer patients and normal controls exhibited a >3.0-fold change in expression level in subjects with cervical cancer, with a P-value of <0.01. In a validation set (n=131) that investigated the expression of 4 of the 6 miRNAs (miR-483-5p, miR-1246, miR-1275 and miR-1290), miR-1290 was found to have significantly higher expression levels in cervical cancer samples (n=45) compared with control samples (n=31). We also found that the median levels of these miRNAs were significantly higher in subjects with cervical cancer (n=45) compared with those in subjects with CIN (n=55). Circulating miRNAs were not correlated with clinicopathological parameters. However, receiver operating characteristic curve analysis suggested that these serum miRNAs may be useful diagnostic markers in cervical cancer. The expression of circulating miR-1290 was significantly higher in the blood of cervical cancer patients compared with that in controls and may thus serve as a useful biomarker in cervical cancer diagnosis. However, larger studies are required to fully elucidate the role of circulating exosomal miRNAs in cervical cancer. [ABSTRACT FROM AUTHOR]