Abstract
Ovarian cancer is the most lethal gynecological malignancy due to its high metastatic ability. Epithelial-mesenchymal transition (EMT) is essential during both follicular rupture and epithelium regeneration. However, it may also accelerate the progression of ovarian carcinomas. Experimental studies have found that 1α,25-dihydroxyvitamin-D3 [1α,25(OH)&sub2;D&sub3;] can inhibit the proliferation of ovarian cancer cells. In this study, we investigated whether 1α,25(OH)&sub2;D&sub3; could inhibit the migration of ovarian cancer cells via regulating EMT. We established a model of transient transforming growth factor-β1(TGF-β1)-induced EMT in human ovarian adenocarcinoma cell line SKOV-3 cells. Results showed that, compared with control, 1α,25(OH)&sub2;D&sub3; not only inhibited the migration and the invasion of SKOV-3 cells, but also promoted the acquisition of an epithelial phenotype of SKOV-3 cells treated with TGF-β1. We discovered that 1α,25(OH)&sub2;D&sub3; increased the expression of epithelial marker E-cadherin and decreased the level of mesenchymal marker, Vimentin, which was associated with the elevated expression of VDR. Moreover, 1α,25(OH)&sub2;D&sub3; reduced the expression level of transcription factors of EMT, such as slug, snail, and β-catenin. These results indicate that 1α,25(OH)&sub2;D&sub3; suppresses the migration and invasion of ovarian cancer cells by inhibiting EMT, implying that 1α,25(OH)&sub2;D&sub3; might be a potential therapeutic agent for the treatment of ovarian cancer.