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Genet Mol Res ; 13(3): 5064-72, 2014 Jul 04.
Article in English | MEDLINE | ID: mdl-25061731

ABSTRACT

5-Azacytidine has been shown to be an effective anti-pancreatic cancer drug, but the mechanism remains unknown. In the current study, we explored the effect of 5-azacytidine on abnormal activation of the Wnt-ß-catenin signaling pathway in pancreatic cancer cells. The human pancreatic cancer cell line Bxpc-3 was treated with different concentrations of 5-azacytidine for various times. The proliferation and early apoptosis of the cells were evaluated using the CCK8 method and flow cytometry, respectively. mRNA and protein expression of ß-catenin, c-myc, and cyclinD1 were detected using real-time fluorescent quantitative polymerase chain reaction and Western blot analysis, respectively. The proliferation of Bxpc-3 cells was suppressed by 5-azacytidine. The early apoptosis of the cells was significantly enhanced over time and with increasing drug concentrations. The expression of ß-catenin, c-myc, and cyclinD1 were down-regulated, showing significant differences between different concentrations and treatment times (P < 0.05). 5-Azacytidine suppressed the proliferation of pancreatic cancer cells by inhibiting the Wnt/ß-catenin signaling pathway, particularly the expression of ß-catenin, c-myc, and cyclinD1. This study may provide a new potential strategy for diagnosing and treating pancreatic cancer.


Subject(s)
Antimetabolites, Antineoplastic/pharmacology , Azacitidine/pharmacology , Cell Proliferation/drug effects , Pancreas/drug effects , beta Catenin/genetics , Cell Line, Tumor , Cyclin D1/antagonists & inhibitors , Cyclin D1/genetics , Cyclin D1/metabolism , Gene Expression Regulation , Humans , Pancreas/metabolism , Pancreas/pathology , Proto-Oncogene Proteins c-myc/antagonists & inhibitors , Proto-Oncogene Proteins c-myc/genetics , Proto-Oncogene Proteins c-myc/metabolism , Signal Transduction , beta Catenin/antagonists & inhibitors , beta Catenin/metabolism
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