摘要
肝细胞癌(HCC)的发病率高、治疗效果差。HCC的发病机制复杂,主要有2类:肝炎、酒精、黄曲霉素、代谢紊乱引起的肝损伤,进而导致的肝硬化;致癌基因和抑癌基因的突变或对应染色体区域的扩增或缺失。细胞内一些信号通路参与了HCC的发生发展,包括RAF/MEK/ERK、PI3K/AKT/mTOR、WNT/β-catenin、胰岛素样生长因子、肝细胞生长因子/c-MET、生长因子调节的血管新生等6类信号通路。抑癌基因通过调节信号通路而调节细胞增殖、细胞周期、细胞凋亡等对肿瘤的发生、发展起重要作用的过程。我们简要概述HCC相关的肿瘤抑制分子及其所在的信号通路及作用的分子机制。
HepatoceUular carcinoma（HCC） is a highly prevalent, treatment-resistant malignancy with a multifacet- ed molecular pathogenesis. Current evidences indicate that during hepatocarcinogenesis, two main pathogenic mecha- nisms prevail： cirrhosis associated with hepatic regeneration after tissue damage caused by hepatitis infection, toxins （for example, alcohol or alflatoxin） or metabolic influences; mutations occurring in single or multiple oncogenes or tumor suppressor genes. Some pathways are involved in the tumorgenesis and development of HCC, including six major pathways： RAF/MEK/ERK pathway, phosphatidylinositol-3 kinase（PI3K）/AKT/mammalian target of rapamycin （mTOR） pathway, Wnt/β-catenin pathway, insulin-like growth factor pathway, hepatocyte growth factor/c-MET path- way and growth factor-regulated angiogenic signaling. Tumor suppressors control tumorgenesis and development by regulating cell proliferatoion, cell cycle, apoptosis and other important process. Here, we systematically reviewed the evidence implicating tumor suppressors in the development of hepatocellular carcinoma and their molecular mechanisms.
出处
《生物技术通讯》
CAS
2012年第6期879-882,共4页
Letters in Biotechnology
基金
国家科技重大专项(2008ZX10002-016)
关键词
抑癌基因
肝细胞癌
信号通路
tumor suppressor
hepatocellular carcinoma
pathway
