Dioscin Inhibits EMT and Invasion of Triple Negative Breast Cancer Cells via Activation of p38MAPK/FOXO3a Signaling

Abstract: The work was aimed to investigate the effect and molecular mechanism of Dioscin on invasion and epithelial to mensenchymal transition (EMT) of triple negative breast cancer cells MDA-MB-231 and BT549. Both cell lines were treated or untreated with Dioscin， normal human epithelial mammary cell line MCF-10A was used as control. Cell proliferation was detected by MTS assay and colony formation assay. The abilities of cell invasion and migration were evaluated by Transwell assay. The expression of p38MAPK， p-p38MAPK， FOXO3a， and EMT-associated biomarkers were analyzed by Western blot. The results showed that the cell proliferation was obviously reduced by Dioscin treatment in a dose dependent manner. Dioscin significantly inhibited the migration of both cells， downregulated the expression of EMT key transcription factor Snail， as well as mesenchymal makers Vimentin and N-cadherin， but increased epithelial marker E-cadherin expression. Moreover， the phosphorylation level of p38MAPK and the expression of FOXO3a were dramatically increased upon Dioscin treatment， and knockdown of FOXO3a reversed the inhibition effects of Dioscin on cell EMT and their invasion and migration capabilities. These above results indicated that Dioscin could inhibit proliferation and mobility of triple negative breast cancer cells in vitro， by which mechanism is related to activation of p38MAPK/FOXO3a signaling.

CSTR: 32200.14.cjcb.2018.05.0002