RhoC is essential in TGF-β1 induced epithelial-mesenchymal transition in cervical cancer cells.

Abstract

Epithelial-mesenchymal transition (EMT) is a critical process in the promotion of epithelial tumor progression and metastasis. The present study aimed to investigate the role of Ras homolog gene family, member C (RhoC) guanosine triphosphatase (GTPase) in transforming growth factor (TGF)-β1 induced EMT. EMT occurred in human cervical carcinoma SiHa cells following TGF-β1 stimulation for 4 days, as demonstrated by the appearance of mesenchymal morphology, reorganization of the actin cytoskeleton, reduced E-cadherin expression and increased Vimentin expression, which was associated with increased RhoC expression and activity. However, EMT was not observed in cells that were pretreated with RhoC siRNA prior to TGF-β1 stimulation. Downregulation of RhoC 4 days following TGF-β1 stimulation was not able to reverse the existing EMT. In addition, TGF-β1 promoted the invasion of the control SiHa cells but not that of the cells in which RhoC was downregulated. In conclusion, RhoC expression is activated by TGF-β1, and sufficient RhoC expression levels are essential for TGF-β1-induced EMT.