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Regulative Mechanism Of PPARγ On The Growth Of Hepatocellular Carcinoma

Posted on:2008-01-05Degree:MasterType:Thesis
Country:ChinaCandidate:H XiaoFull Text:PDF
GTID:2144360215463488Subject:Department of General Surgery
Abstract/Summary:PDF Full Text Request
Objective: To study the effects of peroxisome proliferators-activatedreceptor (PPAR)γactivation on the growth of human hepatocellularcarcinoma cells and explore the role of phosphatase and tensinhomologue deleted on chromosome ten (PTEN) and Phospho-Akt in thisprocess.METHODS: SMMC-7721 cells were treated with 15-d-PGJ2 orpioglitazone, which were two kinds of PPARγligands, at differentconcentrations for indicated time period. The growth of SMMC-7721cells was evaluated by MTT assay. The cell cycle was analyzed by flowcytometry. PTEN and pAkt expressions of SMMC-7721 cells treated with15-d-PGJ2 or pioglitazone, were determined by RT-PCR and Western-blot.RESULTS: MTT assay demonstrated that both 15-d-PGJ2 andpioglitazone had an inhibitory effect on the growth of SMMC-7721 cellsin a time- and dose- dependent manner. According to flow cytometrydetection, more cells were arrested in G0/G1 phase. RT-PCR revealed that the expression of PTEN mRNA was increased in 15-d-PGJ2 orpioglitazone-treated cells. Western-blot analysis confirmed that theexpression of PTEN protein was increased, while pAkt level wasdecreased correspondingly.CONCLUSION: The ligands of PPARγcould inhibit SMMC-7721proliferation in a time- and dose- dependent manner. The upregulation ofPTEN may be involved in the underlying mechanism.
Keywords/Search Tags:Peroxisome proliferators-activated receptors gamma, Carcinoma, Hepatocellular, Phosphatase and tensin homologue deleted on chromosome ten
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