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

肿瘤促进剂Teleosidin能刺激PLC/PRF/5肝癌细胞的蛋白激酶C，这在结构上不同于其他类型的细胞。遥杀素能抑制丝裂霉素C和依托泊苷诱导的肝癌细胞凋亡。Thapsigargin耗尽内质网钙池，诱导肝癌细胞凋亡。Thapsigargin诱导的细胞凋亡与P53核表达增加无关，而丝裂霉素C和依托泊苷诱导的细胞凋亡发生在P53核积聚之前。因此，肿瘤促进剂可能通过调节细胞凋亡过程来促进肿瘤的发生。已经研究了肝炎病毒通过类似的机制促进肝癌发生的可能性。

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.