BACKGROUND AND OBJECTIVES: Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide. The regulator of G-protein signaling 5 (RGS5) has been reported to be highly expressed in some malignant tumors. However, its expression and role in HCC has not been reported. METHODS: The expression of RGS5 was examined in liver cancer tissues and cell lines by real-time quantitative PCR. The cell migration and invasion was investigated by wound healing and transwell invasion assay. The epithelial-mesenchymal transition markers were detected by Western blotting or immunofluorescence. RESULTS: We observed that RGS5 is over-expressed in most of liver cancer tissue samples and cell lines compared with matched normal samples. Further analysis showed that the over-expression of RGS5 is associated with liver cancer recurrence, venous infiltration, and patients' poor survival. Next, we found that knockdown of RGS5 significantly inhibits liver cancer cell migration and invasion in highly invasive liver cancer cells. Furthermore, we found that over-expression of RGS5 induces epithelial-mesenchymal transition in epithelial liver cancer cells. CONCLUSIONS: These results indicate that over-expression of RGS5 promotes tumor metastasis by inducing epithelial-mesenchymal transition in HCC.
BACKGROUND AND OBJECTIVES:Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide. The regulator of G-protein signaling 5 (RGS5) has been reported to be highly expressed in some malignant tumors. However, its expression and role in HCC has not been reported. METHODS: The expression of RGS5 was examined in liver cancer tissues and cell lines by real-time quantitative PCR. The cell migration and invasion was investigated by wound healing and transwell invasion assay. The epithelial-mesenchymal transition markers were detected by Western blotting or immunofluorescence. RESULTS: We observed that RGS5 is over-expressed in most of liver cancer tissue samples and cell lines compared with matched normal samples. Further analysis showed that the over-expression of RGS5 is associated with liver cancer recurrence, venous infiltration, and patients' poor survival. Next, we found that knockdown of RGS5 significantly inhibits liver cancer cell migration and invasion in highly invasive liver cancer cells. Furthermore, we found that over-expression of RGS5 induces epithelial-mesenchymal transition in epithelial liver cancer cells. CONCLUSIONS: These results indicate that over-expression of RGS5 promotes tumor metastasis by inducing epithelial-mesenchymal transition in HCC.
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