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已发表论文

ARHGAP18  过表达通过抑制 MAPK 信号通路的过度激活抑制胃癌中的细胞增殖,迁移,侵袭和肿瘤生长

 

Authors Li Y, Ji S, Fu L, Jiang T, Wu D, Meng F

Received 14 December 2016

Accepted for publication 19 May 2017

Published 9 January 2018 Volume 2018:11 Pages 279—290

DOI https://doi.org/10.2147/OTT.S130255

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Akshita Wason

Peer reviewer comments 3

Editor who approved publication: Prof. Dr. Geoffrey Pietersz

Abstract: Globally, gastric cancer is the second-greatest cause of cancer death. ARHGAP18  belongs to the Rho family of GTPases which is involved in cellular migration, invasion, and growth phases. The aim of the present study was to investigate whether ARHGAP18  could regulate cell proliferation, migration, invasion, and related molecular mechanisms in gastric cancer. Cell Counting Kit-8 (CCK-8) assay results showed that following transfection of a recombinant plasmid, over-expression of ARHGAP18  inhibited cell viability in MGC-803 and BGC823 cells. Using in vitro transwell analysis, migration and invasion abilities were significantly inhibited in cells with high ARHGAP18  expression. Phosphorylation levels of ERK, JNK, and p38 by Western blot analysis significantly declined after transfection of cells with the ARHGAP18  plasmid. Expression levels of ROCK, MTA1, and MMP-2/9 were detected by real-time polymerase chain reaction and Western blotting, and over-expression of ARHGAP18  decreased the expression levels of ROCK, MTA1, and MMP-9. A further in vivo tumor formation study in nude mice indicated that over-expression of ARHGAP18  delayed the progress of tumor formation. These results indicate that ARHGAP18  could act as a tumor suppressor and may serve as a promising therapeutic strategy for gastric cancer.
Keywords: ARHGAP18 , gastric cancer, cell proliferation, migration, invasion, MAPK