Journal
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
Volume 9, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2021.674919
Keywords
RNA modification; METTL3; m6A; Hepatocellular carcinoma; drug-resistance
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Funding
- National Natural Science Foundation of China [81772995, 81472266]
- Excellent Youth Foundation of Jiangsu Province, China [BK20140032]
- Jiangsu Province's Key Provincial Talents Program [ZDRCA2016090]
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Hepatocellular carcinoma (HCC) is the 6th most prevalent cancer globally, and m6A modification may play a role in its pathogenesis. METTL3, a key methyltransferase, is involved in the carcinogenesis and progression of HCC.
Hepatocellular carcinoma (HCC) is the 6th most prevalent cancer and the 4th leading cause of cancer-related death worldwide. Mechanisms explaining the carcinogenesis of HCC are not clear yet. In recent years, rapid development of N-6-methyladenosine (m6A) modification provides a fresh approach to disclosing this mystery. As the most prevalent mRNA modification in eukaryotes, m6A modification is capable to post-transcriptionally affect RNA splicing, stability, and translation, thus participating in a variety of biological and pathological processes including cell proliferation, apoptosis, tumor invasion and metastasis. METTL3 has been recognized as a pivotal methyltransferase and essential to the performance of m6A modification. METTL3 can regulate RNA expression in a m6A-dependent manner and contribute to the carcinogenesis, tumor progression, and drug resistance of HCC. In the present review, we are going to make a clear summary of the known roles of METTL3 in HCC, and explicitly narrate the potential mechanisms for these roles.
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