ArticleWorld journal of gastroenterology2004
The effect of adenovirus expressing wild-type p53 on 5-fluorouracil chemosensitivity is related to p53 status in pancreatic cancer cell lines.
Article in World journal of gastroenterology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 31 citations in OpenAlex.
- Transmission electron microscopic analysis of pancreatic ductal adenocarcinoma cell spheres formed in 3D cultures.Medical molecular morphology · 2025Article
- The p53 reactivator PRIMA-1Investigational new drugs · 2023Article
- Biological activity of PtScientific reports · 2018Article
- Bugs and drugs: oncolytic virotherapy in combination with chemotherapy.Current pharmaceutical biotechnology · 2012Review
- Upregulated p53 expression activates apoptotic pathways in wild-type p53-bearing mesothelioma and enhances cytotoxicity of cisplatin and pemetrexed.Cancer gene therapy · 2012Article
- Proton-shuttling lichen compound usnic acid affects mitochondrial and lysosomal function in cancer cells.PloS one · 2012Article
- Disparate chromatin landscapes and kinetics of inactivation impact differential regulation of p53 target genes.Cell cycle (Georgetown, Tex.) · 2010Article
- Reactivation of p53 by novel MDM2 inhibitors: implications for pancreatic cancer therapy.Current cancer drug targets · 2010Article
- Gene medicine for cancer treatment: commercially available medicine and accumulated clinical data in China.Drug design, development and therapy · 2009Article
- Hsp70 response to 5-fluorouracil treatment in human colon cancer cell lines.International journal of colorectal disease · 2007Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimThere 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.
methodsHuman 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 studies. Following 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.
resultsAd-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 wt-p53. In vivo experiments showed the most effective tumor regression in animals treated with Ad-p53 plus 5-FU. Both in vitro and in vivo analyses revealed that a sublethal dose of Ad-p53 augmented the apoptotic response induced by 5-FU.
conclusionOur results suggest that Ad-p53 may synergistically enhance 5-FU-chemosensitivity most strikingly in pancreatic cancer cells lacking p53 function. These findings illustrate that the anticancer efficacy of this combination treatment is dependent on the p53 gene status of the target tumor cells.
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