Abstract
The objective of the study was to investigate the effects of a Rho-kinase inhibitor on 95D lung carcinoma cell growth, adhesion, invasion, and migration and to explore the underlying molecular mechanisms involved in this process. After treatment of 95D lung carcinoma cells with fasudil, an inhibitor of Rho-kinase, cell biological behaviors such as growth, adhesion, invasion, and migration were observed. Matrix metalloproteinase (MMP) activity and Western blot assay were used to evaluate underlying molecular mechanisms. The IC50 of fasudil to 95D lung carcinoma cells was approximately 0.79mg/mL (95% confidence limits 0.58-1.11mg/mL). After treatment with 0.75mg/mL fasudil, the ability of 95D lung carcinoma cells for growth, adhesion, migration, and invasion was decreased significantly. Total active MMP2 was decreased approximately 22.7% (p< 0.05) and total MMP9 65.9% (p< 0.01). Myosin phosphatase target subunit 1 (MYPT1) was reduced by 29.4% (p< 0.05). We conclude that the Rho-kinase inhibitor prevents the growth, adhesion, invasion, and migration of 95D lung carcinoma cells by inhibiting the Rho/Rho-kinase pathway. Changes in MMP2, MMP9, and MYPT1 may be part of its molecular mechanisms.
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