摘要
c_myc是一个在细胞增殖、分化、凋亡和细胞周期中起重要作用的核内癌基因。c_myc借助c_fos经P38丝裂原蛋白激活酶(P38MAP)通路诱导细胞凋亡。WHV/HBV与细胞染色体整合可激活c_myc基因高表达,从而引起细胞过度增殖迅速形成肝肿瘤。HBx蛋白能够抑制c_myc经P38MAP通路诱导的凋亡。HBx蛋白与c_myc联合作用经人类端粒酶逆转录酶(human telomerase reverese transcriptase,hTERT)途径促进肝细胞癌(HCC)的发生。c_myc可能与HBV相关性HCC有关。
The proto-oncogene c-myc encodes a transcription factor that plays a pivotal role in cell proliferation, differentiation and apoptosis. The signaling mechanism of c-myc-induced apoptosis by c-los increase in the P38 mitogenactivated protein kinase activition. Integration of HBV/WHV DNA within host liver cell chromosomes may be a crucial step in the development of hepatocellular carcinoma. HBx protein can inhibit the c-myc-induced apaptotic signaling in hepatoma cells via the P38 mitogen-activated protein kinase pathway. HBx protein and c-myc cooperation hTERT pathway accelerate hepatocellular carcinoina development, c-myc gene may relate hepatitis B virus-associated hepatocellular careino.
出处
《国际流行病学传染病学杂志》
CAS
2006年第2期112-114,共3页
International Journal of Epidemiology and Infectious Disease
基金
国家自然科学基金(30471518)