Effects of hepatitis virus gene expression on the action of tumor promoters

肿瘤启动子teleocidin对pLC/pRF/5肝癌细胞蛋白激酶C的激活作用与其它类型细胞的蛋白激酶C结构不同。Teleocidin抑制丝裂霉素C和足叶乙甙诱导的肝癌细胞凋亡。毒胡萝卜素能耗竭内质网钙库，诱导肝癌细胞凋亡。毒胡萝卜素诱导的细胞凋亡与细胞核p53的增加无关，而丝裂霉素C和足叶乙甙诱导的细胞凋亡之前，细胞核p53的积累。因此，肿瘤促进剂可通过调节凋亡过程来增强致癌作用。肝炎病毒通过类似的机制促进肝癌发展的可能性已经被研究过。

Tumor promoter teleocidin stimulates protein kinase C of pLC/pRF/5 hepatoma cells which is structurally different from that of other kinds of cells. Teleocidin inhibits apoptosis of the hepatoma cells induced by mitomycin C and etoposide. Thapsigargin depletes endoplasmic reticulum calcium pool, and induces apoptosis of the hepatoma cells. Thapsigargin-induced apoptosis is not associated with an increased nuclear p53, while apoptosis induced by mitomycin C and etoposide is preceded by nuclear p53 accumulation. Therefore, tumor promoters may enhance carcinogenesis by modulating apoptotic processes. A possibility that hepatities viruses enhance hepatoma development by similar mechanism has been studied.