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

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 w...

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Autores principales: Li, Jun-ping, Liu, Yang, Yin, Yi-hua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5308566/
https://www.ncbi.nlm.nih.gov/pubmed/28223826
http://dx.doi.org/10.2147/OTT.S112223
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author Li, Jun-ping
Liu, Yang
Yin, Yi-hua
author_facet Li, Jun-ping
Liu, Yang
Yin, Yi-hua
author_sort Li, Jun-ping
collection PubMed
description 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.
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spelling pubmed-53085662017-02-21 ARHGAP1 overexpression inhibits proliferation, migration and invasion of C-33A and SiHa cell lines Li, Jun-ping Liu, Yang Yin, Yi-hua Onco Targets Ther Original Research 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. Dove Medical Press 2017-02-07 /pmc/articles/PMC5308566/ /pubmed/28223826 http://dx.doi.org/10.2147/OTT.S112223 Text en © 2017 Li et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Original Research
Li, Jun-ping
Liu, Yang
Yin, Yi-hua
ARHGAP1 overexpression inhibits proliferation, migration and invasion of C-33A and SiHa cell lines
title ARHGAP1 overexpression inhibits proliferation, migration and invasion of C-33A and SiHa cell lines
title_full ARHGAP1 overexpression inhibits proliferation, migration and invasion of C-33A and SiHa cell lines
title_fullStr ARHGAP1 overexpression inhibits proliferation, migration and invasion of C-33A and SiHa cell lines
title_full_unstemmed ARHGAP1 overexpression inhibits proliferation, migration and invasion of C-33A and SiHa cell lines
title_short ARHGAP1 overexpression inhibits proliferation, migration and invasion of C-33A and SiHa cell lines
title_sort arhgap1 overexpression inhibits proliferation, migration and invasion of c-33a and siha cell lines
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5308566/
https://www.ncbi.nlm.nih.gov/pubmed/28223826
http://dx.doi.org/10.2147/OTT.S112223
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