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MicroRNA‐373, a new regulator of protein phosphatase 6, functions as an oncogene in hepatocellular carcinoma
Author(s) -
Wu Nannan,
Liu Xuyuan,
Xu Xuemei,
Fan Xingxing,
Liu Min,
Li Xin,
Zhong Qiping,
Tang Hua
Publication year - 2011
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2011.08120.x
Subject(s) - oncogene , microrna , cell cycle , biology , cell growth , downregulation and upregulation , cancer research , cell , regulation of gene expression , microbiology and biotechnology , regulator , gene , genetics
MicroRNAs are a class of small noncoding RNAs that function as key regulators of gene expression at the post‐transcriptional level. Recently, microRNA‐373 (miR‐373) has been found to function as an oncogene in testicular germ cell tumors. In our study, we found that miR‐373 is upregulated in human hepatocellular carcinoma (HCC) tissues as compared with adjacent normal tissues, and promotes the proliferation of the HCC cell lines HepG2 and QGY‐7703 by regulating the transition between G 1 ‐phaseand S‐phase. The gene encoding the protein phosphatase 6 catalytic subunit ( PPP6C ), a negative cell cycle regulator, was identified as a direct target gene of miR‐373 by use of a fluorescent reporter assay. The mRNA and protein levels of PPP6C were both inversely correlated with the miR‐373 expression level. Overexpression of PPP6C abolished the regulation of cell cycle and cell growth exercised by miR‐373 in HepG2 cells. These results indicate that miR‐373 plays an important role in the pathogenesis of HCC, and may be a new biomarker in HCC. Our results demonstrate that miR‐373 can regulate cell cycle progression by targeting PPP6C transcripts and promotes the growth activity of HCC cells in vitro . The downregulation of PPP6C by miR‐373 may explain why the expression of miR‐373 can promote HCC cell proliferation.