Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT01586 (G418)
 2,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Loss of RhoA expression prevents proliferation and metastasis of SPCA1 lung cancer cells in vitro. 2566 83