4.6 Article

Mir-184 Post-Transcriptionally Regulates SOX7 Expression and Promotes Cell Proliferation in Human Hepatocellular Carcinoma

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PLOS ONE
卷 9, 期 2, 页码 -

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PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0088796

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资金

  1. Guangdong Natural Science Foundation [10451130001004472, S2013010016023]
  2. Science and Technology Programme of Guangzhou Municipal Government [2013J4100081]
  3. Supported Foundation of Science and Technology Innovation of Zengcheng [ZC201004]
  4. National Natural Science Foundation of China [81000959]
  5. Science and Technology Planning Project of Guangdong Province, China [2009B030801007]
  6. Fundamental Research Funds for the Central Universities [12ykpy47]
  7. National 12th Five-Year Science and Technology Plan Major Projects of China [2012ZX10002017-005]
  8. National Science Foundation of China [81201781]

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Hepatocellular carcinoma (HCC) is one of the most common human malignancies and the third leading cause of cancer mortality worldwide. The development and progression of HCC is a complicated process, involving the deregulation of multiple genes that are essential to cell biological processes. Recently, microRNAs (miRNAs) have been suggested to be closely associated with tumorigenesis. Our study showed that miR-184 is upregulated in HCC cell lines and tissues. Overexpression of miR-184 in HCC cells increased cell proliferation, tumorigenicity, and cell cycle progression, whereas inhibition of miR-184 reduced cell proliferation, tumorigenicity, and cell cycle progression. Additionally, we identified SOX7 as a direct target of miR-184. Ectopic expression of miR-184 led to downregulation of the SOX7 protein, resulting in upregulation of c-Myc, Cyclin D1, and phosphorylation of Rb. Our findings suggested that miR-184 represents a potential onco-miR and plays an important role in HCC progression by suppressing SOX7 expression.

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