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miR-501 acts as an independent prognostic factor that promotes the epithelial–mesenchymal transition through targeting JDP2 in hepatocellular carcinoma
Hepatocellular carcinoma (HCC), the second common cancer, was a kind of primary liver cancer with high incidence. miR-501, identified as a novel regulator, was acted as a potential biomarker in several diseases. JDP2, acted as a repressor of AP-1 complex, was a member of the basic leucine zipper (bZ...
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Published in: | Human cell : official journal of Human Cell Research Society 2019-07, Vol.32 (3), p.343-351 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Hepatocellular carcinoma (HCC), the second common cancer, was a kind of primary liver cancer with high incidence. miR-501, identified as a novel regulator, was acted as a potential biomarker in several diseases. JDP2, acted as a repressor of AP-1 complex, was a member of the basic leucine zipper (bZIP) transcription factor family. RT-qPCR was applied to evaluate miR-501 and JDP2 expression level and we found that miR-501 was upregulated in HCC tissues and cells. miR-501 ectopic expression promoted HCC cell invasion and epithelial–mesenchymal transition (EMT), while low expression present the opposite results. JDP2 was downregulated in HCC tissues and cells, and overexpressed JDP2 facilitated HCC cell invasion and EMT. Furthermore, luciferase reporter assay indicated that JDP2 was a target of miR-501 and altered miR-501 expression the JPD2 mRNA may changed. The expression of miR-501 and JDP2 had negative connection in HCC tissues. In addition, Kaplan–Meier method revealed that miR-501 upregulation or JDP2 downregulation predicted poor prognosis in HCC patients. miR-501 promoted cell invasion and EMT by regulated JDP2 in hepatocellular carcinoma. The newly identified miR-501/JDP2 axis provides novel insight into the pathogenesis of hepatocellular carcinoma. |
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ISSN: | 1749-0774 0914-7470 1749-0774 |
DOI: | 10.1007/s13577-019-00243-7 |