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HSG Provides The Great Antitumor Efficacy On Hepatocellular Carcinoma Both In Vitro And In Vivo

Posted on:2010-11-17Degree:MasterType:Thesis
Country:ChinaCandidate:S Q WangFull Text:PDF
GTID:2144360275477323Subject:Clinical Medicine
Abstract/Summary:PDF Full Text Request
Aim:Hyperplasia suppressor gene(HSG) is a novel gene that markedly suppresses the mitogenic stimuli or injury mediated vascular smooth muscle cells proliferation and preventing balloon injury induced restenosis.In this study,we provide experimental evidence to confirm the role of HSG as a tumor suppressor gene and investigate its potential in therapeutic applications by using adenovirus vectors.Methods:HSG expression was detected by Western Blot and PCR in hepatocellular cancer tissues as well as in paired adjacent normatic tissues.The HepG2 cells were transfected with an adenoviral vector containing HSG gene and the expression of HSG gene was detected by Western Blot.Effect of HSG on HepG2 cells proliferation were investigated by Western Blot for the expression of cyclin dependent kinase inhibitors (CKIs) and proliferating cell nuclear antigen(PCNA),and by Flow cytometry analysis for cell-cycle distribution and also by Cell Couting Kit-8 for cell viability assay.We also sought to determine whether exogenous HSG affected tumorigenicity both ex vivo and in vivo by nude mice.Results:HSG was downregulated in hepatocellular carcinoma tissues compared to nearby normatic tissues.Overexpression of HSG remarkedly resulted in decreased cell viability and cell cycle arrest in the G0/G1 phase,increased expression of the CKIs,and reduced expression of PCNA.Upregulation of HSG by adenovirus also significantly suppressed the growth of subcutaneous tumors in nude mice both ex vivo and in vivo.Conclusion:Taken together,our data suggest that HSG is an important therapeutic target for the treatment of tumors and possibly other hyper-proliferative diseases as well.
Keywords/Search Tags:Hyperplasia suppressor gene (HSG), hepatocellular cacinoma (HCC), Adenovirus, cell cycle, Cyclin dependent kinase inhibitors (CKIs), p53
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