N6-methyladenosine (m6A) modification in hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is one of the deadliest cancers of human, the tumor-related death of which ranks third among the common malignances. N6­methyladenosine (m6A) methylation, the most abundant internal modification of RNA in mammals, participates in the metabolism of mRNA and interrelates...

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Veröffentlicht in:Biomedicine & pharmacotherapy 2024-04, Vol.173, p.116365-116365, Article 116365
Hauptverfasser: Ma, Hehua, Hong, Yuxin, Xu, Zhenzhen, Weng, Zuyi, Yang, Yuanxun, Jin, Dandan, Chen, Zhiyou, Yue, Jing, Zhou, Xuan, Xu, Zhi, Fei, Fei, Li, Juan, Song, Wei
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Sprache:eng
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Zusammenfassung:Hepatocellular carcinoma (HCC) is one of the deadliest cancers of human, the tumor-related death of which ranks third among the common malignances. N6­methyladenosine (m6A) methylation, the most abundant internal modification of RNA in mammals, participates in the metabolism of mRNA and interrelates with ncRNAs. In this paper, we overviewed the complex function of m6A regulators in HCC, including regulating the tumorigenesis, progression, prognosis, stemness, metabolic reprogramming, autophagy, ferroptosis, drug resistance and tumor immune microenvironment (TIME). Furthermore, we elucidated the interplay between m6A modification and non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs). Finally, we summarized the potential of m6A regulators as diagnostic biomarkers. What’s more, we reviewed the inhibitors targeting m6A enzymes as promising therapeutic targets of HCC. We aimed to help understand the function of m6A methylation in HCC systematically and comprehensively so that more effective strategies for HCC treatment will be developed. [Display omitted] •m6A modification participates in the malignant phenotype of HCC.•The interaction between m6A and ncRNAs plays a noteworthy role in HCC progression.•Targeting m6A regulators is a promising therapeutic strategy for HCC.
ISSN:0753-3322
1950-6007
DOI:10.1016/j.biopha.2024.116365