Diflunisal Promotes Breast Cancer Cells Apoptosis by Regulating the ILP-2/Bcl-2/Bax Signaling Pathway
PENG Hang, XIANG Siqi, JIANG Shuangyan, CUI Ruxia, XIANG Mingjun*
This paper aimed to discuss the effects of diflunisal on the apoptosis of MCF-7 and MDAMB-231 breast cancer cells and its molecular mechanism. CCK-8 assay was applied to detect the effect of different concentrations of diflunisal on breast cancer cell proliferation. The effect of diflunisal on the clone formation of breast cancer cell was detected by plate clone formation. The migration of breast cancer cell was determined by the scratch assay. Apoptosis of breast cancer cell was analyzed by AO-EB (acridine orange/ethidium bromide). The protein expression levels of ILP-2, Bax, Bcl-2 and Cleaved-caspase-3 were detected by WB (Western blot). CCK-8 showed that compared with the control group, the diflunisal group significantly inhibited MCF-7 cells and MDAMB-231 cells, and the inhibition increased with concentration and time. Diflunisal significantly inhibited the migrationability of the cells. The number of apoptotic cells increased, and the apoptosis rate was drug concentrationdependent. Western blot showed upregulation of pro-apoptotic proteins Cleaved-caspase-3 and Bax, and significant downregulation of apoptosis inhibitor protein ILP-2 and anti-apoptotic protein Bcl-2. As the drug concentration increased, the expression level of each protein changed more significantly. Results indicate that diflunisal induces breast cancer cell apoptosis by downregulating ILP-2 protein expression and subsequently affecting the Bcl-2/Bax signaling pathway.
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