MicroRNA‑144 suppresses tumorigenesis of hepatocellular carcinoma by targeting AKT3

Mol Med Rep. 2015 Feb;11(2):1378-83. doi: 10.3892/mmr.2014.2844. Epub 2014 Nov 3.

Abstract

Aberrant expression of microRNAs (miRNAs) has been shown to be associated with the progression and metastasis of cancer. Dysregulation of miR‑144 has been observed in numerous types of cancer; however, the exact role of miR‑144 in hepatocellular carcinoma (HCC) remains unclear. The present study observed that miR‑144 was downregulated in HCC tissues and cell lines. Forced overexpression of miR‑144 suppressed proliferation, migration and invasion of HCC cells. AKT3 was identified as a direct target of miR‑144 in HCC, and this was confirmed by a luciferase activity assay and western blot analysis. Overexpression of AKT3 in miR‑144 transfected HCC cells effectively reversed the tumor suppressive effects of miR‑144. Furthermore, AKT3 expression levels were inversely correlated with miR‑144 expression levels in HCC tissues. In conclusion, the results of the present study suggest that miR‑144 may act as a tumor suppressor in HCC by targeting AKT3, and miR‑144 may be a potential therapeutic candidate for HCC.

MeSH terms

  • 3' Untranslated Regions
  • Base Sequence
  • Carcinogenesis
  • Carcinoma, Hepatocellular / genetics*
  • Carcinoma, Hepatocellular / pathology
  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation
  • Down-Regulation
  • Hep G2 Cells
  • Humans
  • Liver Neoplasms / genetics*
  • Liver Neoplasms / pathology
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Sequence Alignment
  • Transfection

Substances

  • 3' Untranslated Regions
  • MIRN144 microRNA, human
  • MicroRNAs
  • AKT3 protein, human
  • Proto-Oncogene Proteins c-akt