RhoA inhibits apoptosis and increases proliferation of cultured SPCA1 lung cancer cells

Abstract

The Rho kinase pathway has previously been reported to possess a close relationship with the growth, migration and invasion of lung cancer cells. However, the molecular mechanisms underlying the effects of this pathway on lung cancer cells are still elusive. The aim of the present study was to investigate the effects and underlying molecular mechanisms of Ras homolog family member A (RhoA) on the proliferation and apoptosis of SPCA1 lung carcinoma cells. Stable SPCA1 lung cancer cell lines, in which RhoA expression was silenced by small interfering RNA, were isolated following Geneticin screening. Inhibition of RhoA expression significantly decreased the proliferation of SPCA1 lung cancer cells, whereas apoptosis was significantly increased (P<0.01) as determined by the MTS tetrazolium assay and flow cytometry analysis, respectively. At the molecular level, knockdown of RhoA resulted in the significant activation of caspase-3 (P<0.01), and a significant reduction in the levels of phosphorylated signal transducer and activator of transcription (phospho-STAT3; P<0.01), as determined by western blotting. The results suggested that RhoA knockdown prevents cell proliferation and induces apoptosis in SPCA1 lung cancer cells. Furthermore, the underlying mechanisms responsible for these effects may include the activation of caspase-3 and the reduction of phospho-STAT3 levels.