期刊
GENETICS AND MOLECULAR RESEARCH
卷 13, 期 3, 页码 5064-5072出版社
FUNPEC-EDITORA
DOI: 10.4238/2014.July.4.22
关键词
5-Azacytidine; c-Myc; CyclinD1; Pancreatic cancer; Wnt/beta-catenin
资金
- Fundamental Research Funds for the Central Universities [lzujbky-2012-163]
- West Light Foundation of the Chinese Academy of Science [2011-180]
- Gansu Provincial Natural Science Foundation [1208RJZA296]
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-beta-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 beta-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 beta-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/beta-catenin signaling pathway, particularly the expression of beta-catenin, c-myc, and cyclinD1. This study may provide a new potential strategy for diagnosing and treating pancreatic cancer.
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