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• W1991804440 abstract "Objective: To understand the impact of protein kinase B (PKB; Akt) signaling on growth and protection from apoptosis in pancreatic ductal adenocarcinoma models demonstrating differences in PKB activity. Methods: Gemcitabine sensitivity was investigated in a panel of cell lines, characterized by differences in levels of activated PKB. Suppression of PKB activity was achieved with an inhibitor of phosphatidylinositol 3-kinase (wortmannin) and silencing RNA. Results: Enhanced gemcitabine (2′,2′-difluoro-2′-deoxycytidine)-induced cytotoxicity in vitro was achieved with suppression of high PKB activity with wortmannin in BxPC-3, PK-1, and PK-8 cells and silencing RNA targeted to total PKB, rather than PKBβ, in PANC-1 cells. Opposite to gemcitabine sensitivity levels in vitro, the growth of PANC-1 xenografts was inhibited with gemcitabine treatment, whereas BxPC-3 became drug resistant. Monolayer cell cultures reestablished from solid tumors behaved similarly to original cultures, suggesting that the tumor microenvironment has a critical role in determining drug sensitivity. A comparison of transcript profiles of the models indicated that PKB signaling might be modulated by a number of pathways responsive to the tumor hypoxia microenvironment. Conclusions: These results suggested that gemcitabine efficacy involving the PKB pathway depends on PKB activity, its mechanisms of enhanced activity, as well as its function in a signaling network." @default.
• W1991804440 created "2016-06-24" @default.
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• W1991804440 date "2007-10-01" @default.
• W1991804440 modified "2023-10-16" @default.
• W1991804440 title "Dissociation of Gemcitabine Sensitivity and Protein Kinase B Signaling in Pancreatic Ductal Adenocarcinoma Models" @default.
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• W1991804440 doi "https://doi.org/10.1097/mpa.0b013e318095a747" @default.
• W1991804440 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17895832" @default.
• W1991804440 hasPublicationYear "2007" @default.
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