Background: Recent evidence shows that CHD4 is involved in a variety of biological events of tumors. Our aim was to investigate the correlation between CHD4 and oral squamous cell carcinoma (OSCC).
Methods: After CHD4 was screened as a differentially expressed gene in The Cancer Genome Atlas (TGCA) database, the correlations of its expression level with the clinical parameters and prognosis of patients with OSCC were analyzed. The outcomes of the multivariate analysis were used to construct a nomogram, and the accuracy of the model was evaluated with the calibration curve. The GeneMANIA and STRING databases were used to generate network diagrams depicting interactions of genes with CHD4, and heat maps of genes co-expressed with CHD4 were generated using the TCGA database. TargetScan was then used to look into the miRNAs that interact with the 3' untranslated region of CHD4 mRNA. Finally, GSEA enrichment analysis was used to explore the possible mechanism.
Results: The differentially expressed molecule CHD4 was screened by TCGA database for OSCC. CHD4 was overexpressed in OSCC tumor tissues, and OSCC patients with low expression of CHD4 have better OS and DSS. The nomogram had a C-index of 0.575 (0.548-0.602), which indicated some degree of predictive reliability. CHD4 has certain correlation with exons of OSCC related genes, including , , , , , , , , and . According to the TargetScan database, hsa-miR-194-5p is the miRNA that regulates CHD4 upstream the most. GSEA analysis showed that CHD4 may participate in the poor prognosis of OSCC by participating in PI3K/AKT pathway, protein adhesion regulation, MAPK pathway, cytokine and inflammatory response regulation, angiogenesis and platelet regulation.
Conclusions: The decreased expression of CHD4 may indicate a better prognosis in OSCC patients and could serve as a novel predictive biomarker for OSCC. Also, hsa-miR-194-5p was found to contribute to the poor prognosis of OSCC by regulating CHD4 and enhancing tumor anoikis resistance via the PI3K/AKT signaling pathway. These findings suggest that CHD4 might be a therapeutic target for the effective treatment of OSCC.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9929775 | PMC |
http://dx.doi.org/10.21037/atm-22-6332 | DOI Listing |
Cell Rep
December 2024
Laboratory of Genome Integrity, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address:
A significant portion of human cancers utilize a recombination-based pathway, alternative lengthening of telomeres (ALT), to extend telomeres. To gain further insights into this pathway, we developed a high-throughput imaging-based screen named TAILS (telomeric ALT in situ localization screen) to identify genes that either promote or inhibit ALT activity. Screening over 1,000 genes implicated in DNA transactions, TAILS reveals both well-established and putative ALT modulators.
View Article and Find Full Text PDFCell Biochem Funct
January 2025
Department of Rheumatology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) is an increasingly recognized extra-articular manifestations (EAMs) in the RA, with highly morbidity and mortality. The identification of key molecules involved in RA-ILD has a high requirement in clinic, and the role of their transcriptional regulation in the etiology of RA-ILD is great significant for investigation. In this study, we collected the whole peripheral blood samples of RA-ILD and RA only patients to bulk RNA-sequence.
View Article and Find Full Text PDFAtrial fibrillation (AF) is the most common sustained arrhythmia, affecting 59 million individuals worldwide. Impairment of atrial cardiomyocyte (aCM) gene regulatory mechanisms predisposes to atrial fibrillation. The transcription factor TBX5 is essential for normal atrial rhythm, and its inactivation causes loss of aCM enhancer accessibility, looping, and transcriptional identity.
View Article and Find Full Text PDFbioRxiv
November 2024
Laboratory of Genome Integrity, National Cancer Institute, National Institutes of Health, Bethesda, MD, United States.
A significant portion of human cancers utilize a recombination-based pathway, Alternative Lengthening of Telomeres (ALT), to extend telomeres. To gain further insights into this pathway, we developed a high-throughput imaging-based screen named TAILS (Telomeric ALT Localization Screen), to identify genes that either promote or inhibit ALT activity. Screening over 1000 genes implicated in DNA transactions, TAILS revealed both well-established and novel ALT modulators.
View Article and Find Full Text PDFInt J Mol Sci
October 2024
Department of Cancer Immunology, Chair of Medical Biotechnology, Poznan University of Medical Sciences, 60-806 Poznan, Poland.
The interplay between cancer and the immune system has captivated researchers for a long time. Recent developments in cancer immunotherapy have substantiated this interest with a significant benefit to cancer patients. Tumor and immune cells are regulated via a wide range of molecular mechanisms involving intricate transcriptional and epigenetic networks.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!