Loss of RhoA expression prevents proliferation and metastasis of SPCA1 lung cancer cells in vitro

被引:22
|
作者
Yang, Xueying [1 ]
Zheng, Fushuang [1 ]
Zhang, Suning [1 ]
Lu, Jibin [1 ]
机构
[1] China Med Univ, Shengjing Hosp, Dept Thorac Surg, Shenyang 110004, Liaoning, Peoples R China
基金
高等学校博士学科点专项科研基金;
关键词
RhoA; Lung cancer; Molecular mechanisms; MYOSIN PHOSPHATASE; BLADDER-CANCER; PROTEINS; INVASION; GTPASES;
D O I
10.1016/j.biopha.2014.12.004
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Lung cancer is the leading cause of cancer-related death worldwide, mainly due to its highly metastatic properties. Previously, we reported an inverse correlation between Rho-kinase inhibitor and the progression of the lung cancer cells. The purpose of this study was to investigate the effects of RhoA on the proliferation, adhesion, invasion, and migration of SPCA1 lung carcinoma cells and to explore the underlying molecular mechanisms. RNA interference was used to downregulate RhoA expression in these cells. Through G418 screening, we generated SPCA1 lung cancer cell lines with stable RhoA silencing. We then observed the cell behaviour, and used matrix metalloproteinase (MMP) activity and western blot assays to evaluate the underlying molecular mechanisms. The proliferation, adhesion, migration, and invasion of SPCA1 lung cancer cells were decreased after knockdown of RhoA. At the molecular level, the total amounts of active MMP2 and MMP9 were decreased by about 17.21% (P < 0.05) and 45.32% (P < 0.01), respectively. Myosin phosphatase targeting subunit 1 phosphorylation (P-MYPT1) was reduced by 36.16% (P < 0.05). Taken together, our findings show that the knockdown of RhoA prevents proliferation and metastasis in SPCA1 lung cancer cells. Changes in MMP2, MMP9, and P-MYPT1 levels and activity might be some of the molecular mechanisms underlying these effects. Crown Copyright (C) 2014 Published by Elsevier Masson SAS. All rights reserved.
引用
收藏
页码:361 / 366
页数:6
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