Genetic alterations in N6-methyladenosine (m6A) regulatory genes are observed in many cancers. Recent studies have shown that newly identified m6A regulatory gene family (IGF2BPs; IGF2BP1, IGF2BP2, and IGF2BP3) were highly expressed in various types of cancer that stabilize and promote translation of multiple oncogenes, resulting in tumor development, survival and drug resistance. However, the oncogenic roles and prognostic values of IGF2BPs in head and neck squamous cell carcinoma (HNSCC) remain largely unknown. In this study, we examined the m6A regulatory genes alteration, their mRNAs expression and the prognostic values in HNSCC. We also analyzed the interaction network and functional enrichment of m6A regulators. Our results showed that m6A regulatory genes were altered in 41% (205/504) of HNSCC patients, of which was amplified in 20% (101/504) of HNSCC patents and positively correlated with its mRNA expression. Importantly, we have validated the expression of in HNSCC and normal tissue samples. Interestingly, we also found that the was frequently co-amplified with the most common oncogenes in HNSCC patients. In addition, this study found that other m6A regulatory genes such as , and were significantly upregulated in HNSCC samples. Moreover, patients with high expression of , and had poor overall survival (OS) than those with low expression. Therefore, it is evident that IGF2BP family plays a key role in the oncogenesis of HNSCC and might serve as novel prognostic biomarkers and potential therapeutic targets in HNSCC.
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Unlabelled: -methyladenosine (m A) is the most prevalent cellular mRNA modification and plays a critical role in regulating RNA stability, localization, and gene expression. m A modification plays a vital role in modulating the expression of viral and cellular genes during HIV-1 infection. HIV-1 infection increases cellular RNA m A levels in many cell types, which facilitates HIV-1 replication and infectivity in target cells.
View Article and Find Full Text PDFJ Biomed Sci
January 2025
Guangdong Provincial Key Laboratory of New Drug Design and Evaluation, State Key Laboratory of Anti-Infective Drug Discovery and Development, School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou, 510006, China.
Background: Recent studies indicate that N6-methyladenosine (mA) RNA modification may regulate ferroptosis in cancer cells, while its molecular mechanisms require further investigation.
Methods: Liquid Chromatography-Tandem Mass Spectrometry (HPLC/MS/MS) was used to detect changes in mA levels in cells. Transmission electron microscopy and flow cytometry were used to detect mitochondrial reactive oxygen species (ROS).
Toxicology
January 2025
School of Public Health, Dali University, Dali, Yunnan, China; Institute of Preventive Medicine, Dali University, Dali, Yunnan, China. Electronic address:
N-methyladenosine (mA) modification and LncRNAs play crucial regulatory roles in various pathophysiological processes, yet roles of mA modification and the relationship between mA modification and LncRNAs in cadmium-induced oxidative damage of pancreatic β-cells have not been fully elucidated. In this study, mA agonist entacapone and inhibitor 3-deazadenosine were used to identify the effects of mA on cadmium-induced oxidative damage as well as LncRNA changes. Our results indicate that elevated levels of mA modification by entacapone can rescue the cell viability and attenuate the cell apoptosis, while the inhibition levels of mA modification can exacerbate the cell death.
View Article and Find Full Text PDFNat Plants
January 2025
State Key Laboratory of Plant Diversity and Specialty Crops, Institute of Botany, Chinese Academy of Sciences, Beijing, China.
Hydrogen peroxide (HO) functions as a critical signalling molecule in controlling multiple biological processes. How HO signalling integrates with other regulatory pathways such as epigenetic modification to coordinately regulate plant development remains elusive. Here we report that SlALKBH2, an mA demethylase required for normal ripening of tomato fruit, is sensitive to oxidative modification by HO, which leads to the formation of homodimers mediated by intermolecular disulfide bonds, and Cys39 serves as a key site in this process.
View Article and Find Full Text PDFCell Death Discov
January 2025
Department of Hepatobiliary Pancreatic Surgery, The Second Hospital of Jilin University, Changchun, China.
Hepatocellular carcinoma (HCC) is among the most malignant tumors and seriously threatens human health worldwide, and its incidence rate is increasing annually. USP15 is a member of the ubiquitination-specific protease (USP) family, which can regulate protein ubiquitination, thereby affecting their stability, and is dysregulated in many cancers, but its expression and regulatory mechanism in HCC are unclear. The aims of this study were to explore the role and mechanism of USP15 in regulating HCC cell stemness, proliferation, and lenvatinib resistance.
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