- 期刊
Suppression of Tumorigenicity of Human Hepatocellular Carcinoma Cells by Replacing a Mutated P53 Gene
並列摘要
p53 is a tumor suppression associated cellular encoded phosphoprotein. Mutations of the p53 gene have been found frequentely in carcinoma of colon, lung, breast as well as osteogenic sarcoma. Therefore, p53 gene appears to be linked to the development of wide variety of human cancer. Hepatocellular carcinoma (HCC) is one of the most severe cancer in Taiwan, yet is quite poorly understood from a genetic standpoint. To explore the possibility of tumor suppression gene involvement in this neoplasm, p53 expression was examined in eight available human hepatocellular carcinoma cell lines. Two of eight, T2 (a subclone of Hep 3B) and HA22T/VGH, completely lack of p53 expression. To assess the functional consequence of this mutation, wild-type p53 gene and mutated p53 gene expressions were restored in T2 and HA22T/VGH via retroviral-mediated gene transfer. Some important findings were observed in both cell lines. First of all, expression of mutated p53 in T2 and HA22T/VGH have no effect on growth rate and saturation density compared to parental cells. On the other hand, the wild-type p53 slightly inhibits the growth rate and cell crowding of both cells. Furthermore, expression of wild-type p53 can successfully reduce the ability of soft-agar colony formation as well as suppress the tumorigenicity in nude mice of T2 and HA22T/VGH. These results strongly suggest p53 inactivation can play a significant role in the genesis of a common adult neoplasm and the restoration of normal p53-encolde protein in tumor cells has a suppression function of neoplastic phenotype. Further investigation of the possible pathways and mechanisms for p53 gene function in hepatocellular carcinoma cells will extend our understanding of the formation of hepatoma.
延伸閱讀
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