PDF(Pubmed)
Abstract：
Hepatocellular carcinoma (HCC) stands as the prevailing form of primary liver cancer, characterized by a poor prognosis and high mortality rate. A pivotal factor in HCC tumorigenesis is epigenetics, specifically the regulation of gene expression through methylation. This process relies significantly on the action of proteins that modify methylation, including methyltransferases, their associated binding proteins, and demethylases. These proteins are crucial regulators, orchestrating the methylation process by regulating enzymes and their corresponding binding proteins. This orchestration facilitates the reading, binding, detection, and catalysis of gene methylation sites. Methylation ences the development, prolisignificantly influferation, invasion, and prognosis of HCC. Furthermore, methylation modification and its regulatory mechanisms activate distinct biological characteristics in HCC cancer stem cells, such as inducing cancer-like differentiation of stem cells. They also influence the tumor microenvironment (TME) in HCC, modulate immune responses, affect chemotherapy resistance in HCC patients, and contribute to HCC progression through signaling pathway feedback. Given the essential role of methylation in genetic information, it holds promise as a potential tool for the early detection of HCC and as a target to improve drug resistance and promote apoptosis in HCC cells.
摘要：
肝细胞癌（HCC）是原发性肝癌的主要形式，预后差，死亡率高。肝癌肿瘤发生的一个关键因素是表观遗传学，特别是通过甲基化调节基因表达。这个过程很大程度上依赖于修饰甲基化的蛋白质的作用，包括甲基转移酶,它们相关的结合蛋白，和去甲基酶.这些蛋白质是关键的调节剂，通过调节酶及其相应的结合蛋白来协调甲基化过程。这种编排方便了阅读，绑定,检测,和基因甲基化位点的催化。甲基化促进了发展，显著影响，入侵,和肝癌的预后。此外，甲基化修饰及其调控机制激活肝癌肿瘤干细胞的独特生物学特性,例如诱导干细胞的癌症样分化。它们还影响HCC的肿瘤微环境（TME），调节免疫反应，影响肝癌患者的化疗耐药性，并通过信号通路反馈促进HCC进展。鉴于甲基化在遗传信息中的重要作用，它有望作为早期检测HCC的潜在工具，并作为改善耐药性和促进HCC细胞凋亡的靶标。
