Purpose: The aim was to investigate mifepristone effects on endometrial carcinoma and the related mechanism.
Methods: HHUA cells were treated with DMEM containing different concentrations of mifepristone. HHUA cells treated with 100 µmol/L mifepristone were named the Mifepristone group. HHUA cells co-transfected with pcDNA3.1-PI3K and pcDNA3.1-AKT overexpression vectors were treated with 100 µmol/L mifepristone and named the Mifepristone + PI3K/AKT group. mRNA expression was detected by quantitative reverse transcription PCR. Protein expression was performed by Western blot. Cell proliferation was conducted by MTT assay. Wound-healing assay was conducted. Transwell was used to detect cells migration and invasion. Apoptosis detection was performed by flow cytometry.
Results: Mifepristone inhibited HHUA cells proliferation in a dose-dependent manner. Compared with HHUA cells treated with 0 µmol/L mifepristone, HHUA cells treated by 50–100 µmol/L mifepristone had a lower wound-healing rate, a greater number of migrating and invasive cells (P <0.01), as well as a higher percentage of apoptotic cells and Caspase-3 expression (P <0.01). When HHUA cells were treated with 50–100 µmol/L of mifepristone, FAK, p-FAK, p-PI3K and p-AKT relative expression was all significantly lower than HHUA cells treated with 0 µmol/L of mifepristone (P <0.01). Compared with the Mifepristone group, HHUA cells of the Mifepristone + PI3K/AKT group had a lower cell growth inhibition rate and percentage of apoptotic cells (P <0.01).
Conclusion: Mifepristone inhibited HUUA cells proliferation, migration and invasion and promoted its apoptosis by regulation of FAK and PI3K/AKT signaling pathway.
Keywords: Mifepristone, HHUA cells, proliferation, FAK, PI3K/AKT signaling pathway