Mir-184 post-transcriptionally regulates SOX7 expression and promotes cell proliferation in human hepatocellular carcinoma

PLoS One. 2014 Feb 18;9(2):e88796. doi: 10.1371/journal.pone.0088796. eCollection 2014.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Base Sequence
  • Carcinogenesis / genetics
  • Carcinoma, Hepatocellular / pathology*
  • Cell Cycle / genetics
  • Cell Line, Tumor
  • Cell Proliferation
  • Gene Expression Regulation, Neoplastic / genetics*
  • Humans
  • Liver Neoplasms / pathology*
  • MicroRNAs / genetics*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • SOXF Transcription Factors / genetics*

Substances

  • MIRN184 microRNA, human
  • MicroRNAs
  • RNA, Messenger
  • SOX7 protein, human
  • SOXF Transcription Factors

Grants and funding

This work was supported as follows: Study design, data collection and analysis–Guangdong Natural Science Foundation(No. 10451130001004472, No. S2013010016023), Science and Technology Programme of Guangzhou Municipal Government(No.2013J4100081), and the Supported Foundation of Science and Technology Innovation of Zengcheng (No. ZC201004); decision to publish, or preparation of the manuscript–National Natural Science Foundation of China (No. 81000959), Science and Technology Planning Project of Guangdong Province, China (No. 2009B030801007), The Fundamental Research Funds for the Central Universities(No. 12ykpy47), National 12th Five-Year Science and Technology Plan Major Projects of China (No. 2012ZX10002017 -005), and the Youth Project of National Science Foundation of China (No. 81201781).