MicroRNA-98 acts as a tumor suppressor in hepatocellular carcinoma via targeting SALL4
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Wuyuan Zhou1, Benkui Zou2, Lisheng Liu3, Kai Cui1, Jie Gao1, Shuanghu Yuan4, Ning Cong5
1Department of Hepatobillary Surgery, Shandong Cancer Hospital, Jinan, Shandong 250117, P.R. China
2Department of Urology Surgery, Shandong Cancer Hospital, Jinan, Shandong 250117, P.R. China
3Clinical Laboratory, Shandong Cancer Hospital, Jinan, Shandong 250117, P.R. China
4Department of Radiation Oncology, Shandong Cancer Hospital, Jinan, Shandong 250117, P.R. China
5Department of Intervention Therapy, Shandong Cancer Hospital, Jinan, Shandong 250117, P.R. China
Ning Cong, email: [email protected]
Keywords: hepatocellular carcinoma, microRNA-98, tumor suppressor, SALL4
Received: June 22, 2016 Accepted: August 16, 2016 Published: September 22, 2016
MicroRNAs (miRs) are involved in the development and progression of hepatocellular carcinoma (HCC), but the regulatory mechanism of miR-98 in HCC still remains unclear. Here we found that miR-98 was significantly downregulated in HCC tissues compared to matched adjacent normal tissues (ANTs). Low miR-98 expression was associated with tumor size, metastasis, portal vein tumor embolus, and poor overall survival. Ectopic expression of miR-98 decreased the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of HCC cells. SALL4 was identified as a novel target of miR-98, and the protein expression of SALL4 was inhibited by miR-98 in HCC cells. Overexpression of SALL4 reversed the suppressive effects of miR-98 on the malignant phenotypes of HCC cells. Besides, SALL4, upregulated in HCC tissues compared to the matched ANTs, was inversely correlated to the miR-98 levels in HCC tissues. In addition, overexpression of miR-98 markedly suppressed the tumor growth as well as tumor-induced death in nude mice. In summary, miR-98 plays a suppressive role in the proliferation, migration, invasion and EMT of HCC cells, partly at least, via directly inhibition of SALL4. Therefore, the miR-98/SALL4 axis may become a promising therapeutic target for HCC.
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