Chunmei Ji1, Hang Liu2, Qiang Yin3, Hui Li4, Han Gao5. 1. Department of Clinical Laboratory, People's Hospital of Weifang, Weifang, Shandong, People's Republic of China. 2. Department of Interventional Therapy, Yidu Central Hospital of Weifang, Weifang, Shandong, People's Republic of China. 3. Department of Oncology, People's Hospital of Rizhao, Rizhao, Shandong, People's Republic of China. 4. Department of PIVAS, People's Hospital of Zhangqiu, Jinan, Shandong, People's Republic of China. 5. Department of Pathology, Qingdao Municipal Hospital, No. 1 Jiaozhou Road, Shibei District, Qingdao, 266000, Shandong, People's Republic of China. gaohanmed@yeah.net.
Abstract
OBJECTIVES: To clarify the potential biological function of miR-93 and its related molecular mechanism underlying metastasis in human hepatocellular carcinoma (HCC). RESULTS: miR-93 was significantly up-regulated in HCC tissues and was associated with poor 5-year overall survival in HCC patients. Transwell assays showed that over-expression of miR-93 increased HCC cell migration and invasion in vitro. Programmed cell death 4 (PDCD4) was a target gene of miR-93 and miR-93 could down-regulate the expression of PDCD4 by directly targeting its 3'-UTR. The re-expression of PDCD4 could attenuate the HCC cell invasion and migration induced by miR-93, while the knockdown of PDCD4 would promote HCC cell migration and invasion via the epithelial-mesenchymal transition (EMT) pathway. CONCLUSIONS: miR-93 provides new insight into the molecular mechanisms of pathogenesis and progression in HCC and offer a potential therapeutic target for the treatment of HCC patients.
OBJECTIVES: To clarify the potential biological function of miR-93 and its related molecular mechanism underlying metastasis in humanhepatocellular carcinoma (HCC). RESULTS:miR-93 was significantly up-regulated in HCC tissues and was associated with poor 5-year overall survival in HCC patients. Transwell assays showed that over-expression of miR-93 increased HCC cell migration and invasion in vitro. Programmed cell death 4 (PDCD4) was a target gene of miR-93 and miR-93 could down-regulate the expression of PDCD4 by directly targeting its 3'-UTR. The re-expression of PDCD4 could attenuate the HCC cell invasion and migration induced by miR-93, while the knockdown of PDCD4 would promote HCC cell migration and invasion via the epithelial-mesenchymal transition (EMT) pathway. CONCLUSIONS:miR-93 provides new insight into the molecular mechanisms of pathogenesis and progression in HCC and offer a potential therapeutic target for the treatment of HCC patients.