Abstract
Liver cancer is the fifth most common malignant tumor in terms of incidence and the third leading cause of cancer-related mortality globally. Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer. Although great progress has been made in surgical techniques, hepatic artery chemoembolization, molecular targeting and immunotherapy, the prognosis of liver cancer patients remains very poor. N6-methyladenosine (m6A) is the most abundant internal RNA modification in eukaryotic cells and regulates various stages of the RNA life cycle. Many studies have reported that the abnormal expression of m6A-related regulators in HCC represent diagnostic and prognostic markers and potential therapeutic targets. In this review, firstly, we introduce the latest research on m6A-related regulators in detail. Next, we summarize the mechanism of each regulator in the pathogenesis and progression of HCC. Finally, we summarize the potential diagnostic, prognostic and therapeutic value of the regulators currently reported in HCC.
Highlights
Liver cancer is the fifth most common malignant tumor in terms of incidence and the third leading cause of cancer-related mortality globally [1]
Increasing attention has been paid to the roles of m6A modification and dysregulated m6A-related regulators in m6A Methylation in Hepatocellular Carcinoma
We focused on the function of m6A RNA modification in hepatocellular carcinoma (HCC)
Summary
Liver cancer is the fifth most common malignant tumor in terms of incidence and the third leading cause of cancer-related mortality globally [1]. Liu et al [83] reported that FTO is negatively regulated by the deacetylase SIRT1 via RANBP2-mediated SUMOylation; its downregulation reduces the expression of its target gene guanine nucleotide-binding protein G(O) subunit alpha (GNAO1), thereby promoting the progression of liver cancer. A subsequent study revealed that FTO might target Cul4a mRNA to downregulate CUL4A protein, thereby presumably blocking HCC cell cycle progression and proliferation [84].
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