期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 288, 期 6, 页码 4035-4047出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M112.410506
关键词
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资金
- National Natural Science Foundation of China [31270818, 91029714, 31071191]
- Natural Science Foundation of Tianjin [12JCZDJC25100, 09JCZDJC17500]
- 211 Project Innovation Foundation of Tianjin Medical University [2010GSI12]
MicroRNAs (miRNAs) are considered to be regulators of various biological processes in cancers, including the epithelial to mesenchymal transition (EMT), which is a key factor in cancer metastasis. In this study, we aimed to clarify the potential roles of miR-490-3p in hepatocellular carcinoma (HCC) cells. Using real-time quantitative RT-PCR, we discovered that miR-490-3p was up-regulated in HCC tissues and cells compared with the adjacent non-tumor tissues and normal cells. We also found that overexpression of miR-490-3p led to an increase in cell proliferation, migration, and invasion abilities and that it contributed to EMT. The inhibition of miR-490-3p had the opposite effect on the cells. We identified ERGIC3 (endoplasmic reticulum-Golgi intermediate compartment protein 3) as a direct target gene for miR-490-3p. Unlike most miRNA-mRNA interactions, miR-490-3p increased ERGIC3 mRNA and protein levels as well as the intensity of expression of the EGFP reporter gene controlled by the 3'-UTR of ERGIC3 mRNA. The up-regulation by miR-490-3p also required the participation of Ago2. The inhibition of miR-490-3p reduced the expression of ERGIC3. Overexpression of ERGIC3 led to the same effect on HCC cells as miR-490-3p overexpression, including EMT. Importantly, silencing ERGIC3 reversed the cellular responses mediated by miR-490-3p overexpression. In conclusion, our study indicated for the first time that miR-490-3p functioned like an oncogenic miRNA in HCC cells and that the inhibition of miR-490-3p might provide an potential treatment approach for HCC patients.
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