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ARHGAP1 overexpression inhibits proliferation, migration and invasion of C-33A and SiHa cell lines

Authors Li JP, Liu Y, Yin YH

Received 6 May 2016

Accepted for publication 10 August 2016

Published 7 February 2017 Volume 2017:10 Pages 691—701

DOI https://doi.org/10.2147/OTT.S112223

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 4

Editor who approved publication: Dr William Cho

Jun-ping Li,1 Yang Liu,2 Yi-hua Yin3

1Department of Gynecology and Obstetrics, Huashan Hospital North, 2Institute of Antibiotics, Huashan Hospital, Fudan University, 3Department of Gynecology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, People’s Republic of China

Abstract: ARHGAP1, also known as RhoGAP, RhoGAP1, CDC42GAP and p50rhoGAP, is officially named Ras homology (Rho) GTPase-activating protein 1, which is one of the key members of RhoGAPs. Growing evidences demonstrate that several RhoGAPs are suppressed or downregulated in cancers. Thus, the aim of this study was to explore the effects of ARHGAP1 on cervical carcinoma cells. The human cervical carcinoma cells C-33A and SiHa were transduced with lentivirus targeting ARHGAP1 (lenti-ARHGAP1). Cellular proliferation, migration and invasion assays, as well as quantitative real-time polymerase chain reaction and Western blot assays, were performed in the control, negative control (infected with lentivirus) and ARHGAP1+-infected groups. Results showed that overexpression of ARHGAP1 markedly inhibited the proliferation of both C-33A and SiHa cells at 24 h, 48 h and 72 h in a time-dependent manner (n=3, P<0.01). Migration and invasion of C-33A and SiHa cells were suppressed after the transduction with lenti-ARHGAP1 compared with the controls (n=3, P<0.01). In addition, several tumor cellular process-related proteins, such as matrix metallopeptidase 2, zinc finger E-box binding homeobox 1, Cyclin B1, twist family bHLH transcription factor 1 and proliferating cell nuclear antigen, were all downregulated in ARHGAP1-overexpressed C-33A and SiHa cells and proved to be targets of ARHGAP1. This study indicated that ARHGAP1 may have a positive function on antitumor activity in the treatment of cervical cancer.

Keywords: cervical carcinoma, ARHGAP1, tumor cellular process-related protein

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