Downregulation of TNFRSF19 and RAB43 by a novel miRNA, miR-HCC3, promotes proliferation and epithelial-mesenchymal transition in hepatocellular carcinoma cells.

Tumor necrosis factor receptor superfamily 19 (TNFRSF19) is a transmembrane protein involved in tumorigenesis. RAB43 is a small molecule GTP-binding protein contributing to the occurrence and development of tumors. However, TNFRSF19/RAB43 dysregulation and their role in hepatocellular carcinoma cells are unknown. Herein, we found that TNFRSF19 and RAB43 were downregulated in hepatocellular carcinoma tissues. TNFRSF19/RAB43 overexpression suppressed, whereas TNFRSF19/RAB43 knockdown promoted cell proliferation and epithelial-mesenchymal transition (EMT) of hepatocellular carcinoma cells. Previously, using deep sequencing technology, a new miRNA, miR-HCC3, was identified and found to suppress the expression of TNFRSF19 and RAB43 by binding to their 3'untranslated regions (3'UTRs) directly. miR-HCC3 was upregulated in hepatocellular carcinoma (HCC) tissues compared with adjacent noncancerous tissues and promoted proliferation and epithelial-mesenchymal transition in HCC cells. Furthermore, TNFRSF19/RAB43 suppressed but miR-HCC3 promoted tumor growth in vivo. Collectively, our results indicated that downregulation of TNFRSF19 and RAB43 by miR-HCC3 contributes to oncogenic activities in HCC, which sheds light on tumorigenesis and might provide potential therapeutic targets for HCC.

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