GANT 61 up-regulates E-cadherin expression and inhibits EMT and invasion of breast cancer cells

With the improvement of breast cancer diagnosis and treatment technology, the mortality rate of breast cancer is reduced to a certain extent, but the recurrence and metastasis rates are still high. The pathogenic factors are related to epithelial-mesenchymal transition (EMT) and breast cancer cell invasion. The Gli inhibitor GANT61 is used for treating several tumors. However, its role in breast cancer EMT and invasion, and related mechanisms have not been reported. The breast cancer cell line MCF-7 was cultured in vitro and randomly divided into control group and GANT61 treatment groups (20, 40, 60 mu mol/L), followed by analysis of cell proliferation using tetrazolium salt colorimetric (MTT) method, cell cycle by flow cytometry, cell apoptosis using Capase-3 activity assay, MMP-9 expression by real-time PCR, and cell invasion by transwell chamber. GANT61's effect on the expression of E-cadherin was detected by Western blot. Compared with control group, GANT61 significantly decreased the proliferation of MCF-7 cells, cell cycle arrest, increased Capase-3 activity, inhibited cell invasion, reduced MMP-9 expression and elevated E-cadherin expression (all P < 0.05) in a dose-dependent manner. GANT61 promotes apoptosis, regulates cell cycle, and inhibits cell proliferation and invasion of breast cancer cells by promoting E-cadherin expression.