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Head and neck squamous cell carcinoma (HNSCC) is a common malignant tumour. Despite advancements in surgery, radiotherapy and chemotherapy, which have improved the prognosis of most patients, a subset of patients with poor prognoses still exist due to loss of surgical opportunities, postoperative recurrence, and metastasis, among other reasons. The tumour microenvironment (TME) is a complex organization composed of tumour, stromal, and endothelial cells. Communication and interaction between tumours and immune cells within the TME are increasingly being recognized as pivotal in inhibiting or promoting tumour development. Previous studies on T cells in the TME of HNSCC have yielded novel therapeutic possibilities. However, the function of B cells, another adaptive immune cell type, in the TME of HNSCC patients has yet to be determined. Recent studies have revealed various distinct subtypes of B cells and tertiary lymphoid structures (TLSs) in the TME of HNSCC patients, which are believed to impact the efficacy of immune checkpoint inhibitors (ICIs). Therefore, this paper focuses on B cells in the TME to explore potential directions for future immunotherapy for HNSCC. [ABSTRACT FROM AUTHOR]

Dachshund family transcription factor 1 (DACH1) has been shown to exhibit a tumour‐suppressive role in a number of human cancers. However, the role of DACH1 in hypopharyngeal squamous cell carcinoma (HPSCC) and its function in the tumour microenvironment (TME) are still not clear. Crosstalk between cancer cells and tumour‐associated macrophages (TAMs) mediates tumour progression in HPSCC. The expression of DACH1, CD86 and CD163 was detected in 71 matched HPSCC–non‐cancerous tissue pairs using quantitative real‐time polymerase chain reaction and IHC analysis. Cell proliferation, migration and invasion were monitored by colony formation, Transwell and EdU incorporation assays. ChIP‐qPCR and dual‐luciferase reporter assays were applied to verify the targeting relationships between DACH1 and IGF‐1. Stably transfected HPSCC cells were co‐cultured with MΦ macrophages to assess macrophage polarization and secretory signals. DACH1 was decreased in HPSCC tissues and was indicative of a poor prognosis for HPSCC patients. Decreased DACH1 expression in HPSCC was associated with fewer CD86+ TAMs and more CD163+ TAMs. Knockdown of DACH1 inhibited the proliferation, migration and invasion of FaDu cells via Akt/NF‐κB/MMP2/9 signalling. Additionally, DACH1 was found to directly bind to the promoter region of IGF‐1 to downregulate the secretion of IGF‐1, which inhibited TAMs polarization through the IGF‐1R/JAK1/STAT3 axis. Furthermore, in nude mice, the effects of DACH1 inhibition on tumour progression and M2‐like TAMs polarization were confirmed. These findings suggest that IGF‐1 is a critical downstream effector of DACH1 that suppresses cell migration and invasion and inhibits TAMs polarization. DACH1 could be a therapeutic target and prognostic marker for HPSCC. [ABSTRACT FROM AUTHOR]

Breast cancer is the most common cause of cancer‑associated mortality and the most frequently diagnosed type of cancer in women worldwide. It has been revealed that the chemokine C‑X‑C motif chemokine ligand 13 (CXCL13) serves a pivotal role in breast cancer growth and is associated with lymph node metastasis. However, to the best of our knowledge, the mechanism by which CXCL13 mediates breast cancer growth remains uncharacterized. Female BALB/c mice were used in this study. Tumor volume was calculated and changes of gross tumor morphology were observed by hematoxylin and eosin staining. The expression of CXCL13, C‑X‑C motif chemokine receptor 5 (CXCR5) and extracellular signaling‑related kinase (ERK) mRNA and protein expression were detected by reverse transcriptase quantitative‑polymerase chain reaction and western blot analysis. Simultaneously, the production of cytokines [interleukin‑1β (IL‑1β), tumor necrosis factor (TNF) and tumor growth factor β1 (TGF‑β1)] was detected by an ELISA. The CXCL13 inhibitor reduced tumor volume and growth, and reduced the mRNA and protein expression levels of key members of the CXCR5/ERK signaling pathway: CXCL13, CXCR5 and ERK. Furthermore, the detectable concentration of the cytokines IL‑1β and TNF decreased following CXCL13 inhibition, whereas the concentration of TGF‑β1 was increased. The attenuation of tumor growth resulting from CXCL13 inhibition may be associated with the CXCR5/ERK signaling pathway. This study provides a theoretical basis for treating breast cancer through CXCL13 inhibition in clinical trials. [ABSTRACT FROM AUTHOR]

In the past decades, the tricyclic acridone ring system has become a focus of major research by medicinal chemists due to the biological significance of this moiety in drug design and discovery. Acridone has substantial bio-potential since it performs crucial functions, including antibacterial, antimalarial, antiviral and anti-neoplastic activities. However, the anticancer effect and the underlying mechanisms of acridone on breast cancer cells remains unclear. In the present study, the anti-tumor function and the underlying mechanisms of acridone were evaluated in vitro. Firstly, an MTT assay was used to evaluate the inhibitory effect of acridone. Subsequently, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to investigate whether ATP binding cassette subfamily G member 2 (ABCG2) was associated with the function of acridone. Finally, western blotting was used to confirm the results of RT-qPCR. The present study demonstrated that acridone may decrease the proliferation of MDA-MB-231 cells dose-dependently. Further experiments revealed that acridone may downregulate the mRNA and protein expression levels of ABCG2, supporting the potential application of acridone in breast cancer treatment. These findings suggested that acridone is a potential agent in the treatment of human breast cancer. [ABSTRACT FROM AUTHOR]

Simple Summary: In recent years, the incidence of cancer has been steadily increasing, necessitating a more urgent and in-depth understanding and exploration of this disease. During the process of literature review, we have discovered that the novel protein-coding gene, cartilage intermediate layer protein 2, has been partially associated with colorectal cancer in several studies. However, its role in other cancers remains elusive. Therefore, this study aims to explore the function and mechanism of cartilage intermediate layer protein 2 in pan-cancer. Our findings will enhance the understanding of the role of cartilage intermediate layer protein 2 in pan-cancer tumorigenesis and progression, especially in pancreatic cancer. This research could potentially establish cartilage intermediate layer protein 2 as a promising prognostic biomarker and immunotherapy target for cancers. The elucidation of its significance in pan-cancer will contribute to the development of more effective therapeutic strategies. Cartilage intermediate layer protein 2 (CILP2) facilitates interactions between matrix components in cartilage and has emerged as a potential prognostic biomarker for cancer. This study aimed to investigate the function and mechanisms of CILP2 in pan-cancer. We evaluated the pan-cancer expression, methylation, and mutation data of CILP2 for its clinical prognostic value. Additionally, we explored the immunological characteristics of CILP2 in pan-cancer and then focused specifically on pancreatic ductal adenocarcinoma (PAAD). The subtype analysis of PAAD identified subtype-specific expression and immunological characteristics. Finally, in vitro and in vivo experiments assessed the impact of CILP2 on pancreatic cancer progression. CILP2 exhibited high expression in most malignancies, with significant heterogeneity in epigenetic modifications across multiple cancer types. The abnormal methylation and copy number variations in CILP2 were correlated with poor prognoses. Upregulated CILP2 was associated with TGFB/TGFBR1 and more malignant subtypes. CILP2 exhibited a negative correlation with immune checkpoints in PAAD, suggesting potential for immunotherapy. CILP2 activated the AKT pathway, and it increased proliferation, invasion, migration, and epithelial–mesenchymal transition (EMT) in pancreatic cancer. We demonstrated that CILP2 significantly contributes to pancreatic cancer progression. It serves as a prognostic biomarker and a potential target for immunotherapy. [ABSTRACT FROM AUTHOR]

Although surgery is an important treatment for laryngeal cancer, surgery has a significant negative impact on the quality of life of patients, and many patients have poor tolerance to surgery. Therefore, alternative chemotherapeutic drugs are an important research hotspot. Chidamide is a histone deacetylase inhibitor that selectively inhibits the expression of type I and IIb histone deacetylases (1, 2, 3 and 10). It has a significant anticancer effect on a variety of solid tumours. This study verified the inhibitory effect of chidamide on laryngeal carcinoma. We conducted a variety of cellular and animal experiments to explore how chidamide inhibits the development of laryngeal cancer. The results showed that chidamide had significant antitumour activity against laryngeal carcinoma cells and xenografts and could induce cell apoptosis, ferroptosis and pyroptosis. This study provides a potential option for the treatment of laryngeal cancer. [Display omitted] [ABSTRACT FROM AUTHOR]

CREPT (also known as RPRD1B) function as an oncogene and is highly expressed in several kinds of cancers. However, the distribution and clinical significance of CREPT in breast cancer (BC) still not clarified. In this study, we found that the CREPT expression is greatly upregulated in BC tissues and cell lines. Moreover, the CREPT expression was significantly associated with tumor differentiation and metastasis. Next, the functional assay of CREPT showed that CREPT could promote BC proliferation and invasion both in vitro and in vivo. Dual-luciferase reporter assay indicated that miR-138 regulated the expression of CREPT by binding to its 3′-UTR. miR-138 is downregulated and inversely correlated with CREPT expression in BCs. Overexpression of miR-138 suppressed tumor growth and invasion, these effects could be reversed by re-expressing CREPT. Mechanistically, CREPT regulated β-catenin/TCF4/cyclin D1 pathway in BC. In conclusion, the data suggested that miR-138/CREPT involved BC progression, providing potential therapeutic targets for BC. [ABSTRACT FROM AUTHOR]

Non-alcoholic fatty liver disease (NAFLD) and its more advanced stages, Non-alcoholic steatohepatitis and Cirrhosis, are the most common liver diseases in the worldwide, especially in developing countries. NAFLD is distinguished by the accumulation of triglycerides within hepatocytes. An increasing body of evidence suggests that hepatic MicroRNAs play an important role in NAFLD by controlling lipid metabolism, inflammation, and fibrosis. However, the precise causative functions of miRNA in NAFLD remain unknown. Here, we discovered that mice lacking MicroRNA-23b developed NAFLD-like phenotypes such as increased serum triglyceride and lipid droplet accumulation. In db/db mice fed a high fat diet, MicroRNA-23b overexpression reduced liver weight and alleviated liver inflammation, apoptosis, and fibrosis. MicroRNA-23b regulates the acyl-CoA metabolic process via Acyl-CoA thioesterase 4 (Acot4), which interacts with Acetyl CoA Carboxylase (ACC), according to the RNA-seq analysis. [ABSTRACT FROM AUTHOR]