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Studies Of The TGF-β1-Responsive Drug-Resistance In Ductal Adenocarcinoma Of Pancreas

Posted on:2007-11-12Degree:MasterType:Thesis
Country:ChinaCandidate:H H ZhaoFull Text:PDF
GTID:2144360182991600Subject:Pathology
Abstract/Summary:PDF Full Text Request
Researches have demonstrated that mdrl was the major reason of Multiple-drug resistance in pancreatic carcinoma. PKC α acts as an important modulator of mdrl. Our previously study has found TGF β 1 can up-regulating PKC α protein. In order to demonstrate the MDR mechanism of pancreatic carcinoma,we use tissue arrayer and immunohistochemistry to observe the relationships among the expressions of TGF β 1,PKC α and P-gp proteins. At the same time we detected the expression of PKC α and P-gp in pancreatic carcinoma cells(BxPC3) with Western-blot after stimulated with TGF- β 1. MTT assay was used to observe the sensitivity of BxPC3 cell to anti-cancer drug cisplatin to detect the influence of TGF- β 1 .Conclusions: Overexpression of TGF- β 1 in pancreatic carcinoma may contribute to the membrane tranfer of PKC α .TGF- β 1 can enhance the expressions of PKC α and P-gp proteins in pancreatic cancer cell line BxPC3 and may aggratate the drug-resistance of pancreatic cancer cells.
Keywords/Search Tags:exocrine pancreatic carcinoma, tissue arrayer, multidrug resistance gene, origin drug-resistance, phenotype, protein kinase C, transforming growth factor, Immunohistochemistry, suppression subtractive hybridization, western-bloting, MTT
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