期刊
ONCOTARGETS AND THERAPY
卷 11, 期 -, 页码 -出版社
DOVE MEDICAL PRESS LTD
DOI: 10.2147/OTT.S154416
关键词
microRNA; HCC; TGF-beta; EMT
资金
- Natural Science Foundation of Guangdong Province [2016A030313195, 2014A030313131]
- Key Scientific and Technological Projects of Guangdong Province [2014B020228003, 2014B030301041]
- Science and Technology Planning Project of Guangzhou [201400000001-3, 158100076]
Introduction: Hepatocellular carcinoma (HCC) accounts for more than 90% of primary liver cancer. Although great progress has been made on HCC molecular mechanism and therapy techniques, the prognosis of HCC patient is poor due to high metastasis and recurrence. Materials and methods: Expression of miR-542-3p was quantified by quantitative real-time PCR (qRT-PCR). The role of miR-542-3p in HCC metastasis was examined using transwell and 3D-culture assay. qRT-PCR, Western blotting and luciferase reporter assay were used to elucidate the mechanisms of miR-542-3p-mediated cancer metastasis. Results and Conclusion: In the research, we found that miR-542-3p is decreased in HCC cell lines and tissues, and downregulation of miR-542-3p enhances, while upregulation suppresses HCC cell invasion ability. Further assay demonstrated that miR-542-3p can directly target TGF-beta 13' untranslated region(3'UTR) to influence TGF-beta/Smad signaling pathway, and suppression of miR-542-3p can hyperactivate TGF-beta/Smad pathway and further to promote Epithelial- Mesenchyme Transition (EMT) and induce poor prognosis. Lastly, the clinical correlation analysis illustrated that miR-542-3p is negatively related with the activity of TGF-beta 1. In summary, our results find that miR-542-3p takes an important role on HCC progression and provide more evidence of microRNAs ( miRNAs) for cancer therapy.
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