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1.
Virologica Sinica ; (6): 226-231, 2008.
Article in Chinese | WPRIM | ID: wpr-407124

ABSTRACT

To explore the role of Human papillomavirus (HPV) in mammary carcinogenesis, the expression of the HPV-16, iNOS, P53 and hTERT proteins in breast carcinomas and their relationships were investigated. 52 samples of breast cancer and 16 samples of benign breast tumors were assayed using the immunohistochemical SP method for detection of protein expression levels. The expression of HPV-16, iNOS, P53 and hTERT proteins in a mammary carcinoma was 44.2%, 57.7%, 63.5% and 59.6% respectively, which was significantly greater than the corresponding levels in the benign group. The expression of iNOS, P53 and hTERT was correlated with the presence of an HPV-16 infection in a mammary carcinoma (P<0.05). The connection between these events might also involve the iNOS, mutated type P53 and the hTERT protein.

2.
Medical Journal of Chinese People's Liberation Army ; (12)2001.
Article in Chinese | WPRIM | ID: wpr-560324

ABSTRACT

Objective To probe the mechanism of hepatocarcinoma cell apoptosis promoted by human telomerase reverse transcriptase (hTERT) RNA interference (RNAi) by mitochondrial pathway in vitro. Methods Westernblot was employed to detect the intracellular expressions of caspase-9, hTERT, Bcl-2 and Bax, and mitochondrial and cytoplastic cytochrome C (cyt C) in HepG2 cells transfected by pSliencer 3.1-H1 neo-shTERT (small hairpin RNA hTERT). Result In the HepG2 cells transfected by pSliencer 3.1-H1 neo-shTERT, expressions of hTERT, Bcl-2 and mitochondrial cyt C were significantly down-regulated, while Bax and cytoplastic cyt C were obviously up-regulated, and active caspase-9 was found in addition to procaspase-9 compared with that in negative control cells and untransfected cells. Conculsion hTERT RNAi may suppress hTERT expression to result in reduction of Bcl-2 and increase of Bax, and then induce hepatocarcinoma HepG2 cell apoptosis by mitochondrial pathway subsequent to cyt C release from mitochondria to cytoplast.

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