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The effect of adenovirus expressing wild-type p53 on 5-fluorouracil chemosensitivity is related to p53 status in pancreatic cancer cell lines

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World Journal of Gastroenterology 2004年第24期10卷 3583-3589页

作者： sven eisold Michael Linnebacher EduardRyschich DaliborAntolovic UlfHinz Ernst Klar Jan Schmidt Department of General Surgery Thoracic and Vascular SurgeryUniversity of RostockSchillingallee 35D-18057 RostockGermany Molecular Pathology University of HeidelbergINFD-68120 HeidelbergGermany Department of General Surgery University of HeidelbergINFD-69120 HeidelbergGermany

AIM:There are conflicting data about p53 function on cellular sensitivity to the cytotoxic action of 5-fluorouracil (5-FU). Therefore the objective of this study was to determine the combined effects of adenovirus-mediated wild-type (wt) p53 gene transfer and 5-FU chemotherapy on pancreatic cancer cells with different p53 gene status. METHODS:Human pancreatic cancer cell lines Capan-1^(p53mut), Capan-2^(p53wt),FAMPAC^(p53mut),PANC1^(p53mut),and rat pancreatic cancer cell lines AS^(p53wt) and DSL6A^(p53null) were used for in vitro *** infection with different ratios of Ad- p53-particles (MOI) in combination with 5-FU,proliferation of tumor cells and apoptosis were quantified by cell proliferation assay (WST-1) and FACS (PI-staining).In addition,DSL6A syngeneic pancreatic tumor cells were inoculated subcutaneously in to Lewis rats for in vivo studies. Tumor size,apoptosis (TUNEL) and survival were determined. RESULTS:Ad-p53 gene transfer combined with 5-FU significantly inhibited tumor cell proliferation and substantially enhanced apoptosis in all four cell lines with an alteration in the p53 gene compared to those two cell lines containing *** vivo experiments showed the most effective tumor regression in animals treated with Ad-p53 plus *** in vitro and in vivo analyses revealed that a sublethal dose of Ad-p53 augmented the apoptotic response induced by 5-FU. CONCLUSION:Our results suggest that Ad-p53 may synergistically enhance 5-FU-chemosensitivity most strikingly in pancreatic cancer cells lacking p53 *** findings illustrate that the anticancer efficacy of this combination treatment is dependent on the p53 gene status of the target tumor cells.

关键词： Adenoviridae Adult Animals Antimetabolites, Antineoplastic Apoptosis Cell Division Cell Line, Tumor Combined Modality Therapy Drug Resistance, Neoplasm Female Fluorouracil Gene Expression Regulation, Neoplastic Gene Therapy Humans In Vitro Male Pancreatic Neoplasms Rats Rats, Inbred Lew Transduction, Genetic Tumor Suppressor Protein p53

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