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Mifepristone inhibits proliferation, migration and invasion of HUUA cells and promotes its apoptosis by regulation of FAK and PI3K/AKT signaling pathway

Authors Sang L, Lu D, Zhang J, Du S, Zhao X

Received 2 April 2018

Accepted for publication 4 July 2018

Published 4 September 2018 Volume 2018:11 Pages 5441—5449


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr XuYu Yang

Lin Sang,1 Dawei Lu,1 Jun Zhang,2 Shihua Du,1 Xingbo Zhao3

1Department of Obstetrics and Gynecology, The Second People’s Hospital of Hefei City Affiliated to Anhui Medical University, Hefei City, Anhui Province, People’s Republic of China; 2Department of Obstetrics, Tai’an City Central Hospital, Tai’an City, Shandong Province, People’s Republic of China; 3Department of Obstetrics and Gynecology, Shandong Provincial Hospital Affiliated to Shandong University, Ji’nan City, Shandong Province, People’s Republic of China

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.

Mifepristone, HHUA cells, proliferation, FAK, PI3K/AKT signaling pathway

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