Myocyte enhancer factor 2D promotes tumorigenicity in malignant glioma cells

Tumour Biol. 2016 Jan;37(1):601-10. doi: 10.1007/s13277-015-3791-6. Epub 2015 Aug 4.

Abstract

The prognosis of patients with malignant glioma is always quite poor, and this poor prognosis is probably due to our incomplete understanding of the molecular mechanisms underlying malignant glioma. It is known that myocyte enhancer factor-2D (MEF2D) plays an oncogenic role in hepatocellular carcinoma and promotes the survival of various types of cells. However, little is known about the expression profile and function of MEF2D in malignant glioma. In this study, we investigated the function and expression of MEF2D in malignant glioma. We found that in malignant glioma, there is an aberrantly high expression of MEF2D, which leads to poor prognosis of malignant glioma. The downregulation of MEF2D suppresses the proliferation of malignant glioma cell lines by inducing delay of S and G2/M phases of cell cycle and promoting apoptosis. Furthermore, the overexpression of MEF2D in astrocytes accelerates cell proliferation by regulating cell cycle progression. Furthermore, a mouse malignant glioma model demonstrated that MEF2D deficiency blocks malignant glioma formation in vivo. We conclude that MEF2D may act as a potential oncogene in malignant glioma and thus serve as a candidate target for malignant glioma therapy.

Keywords: Apoptosis; Cell cycle; MEF2D; Malignant glioma.

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Astrocytes / metabolism
  • Cell Cycle / genetics
  • Cell Line, Tumor
  • Cell Proliferation
  • Cell Transformation, Neoplastic / genetics*
  • Cell Transformation, Neoplastic / metabolism
  • Disease Models, Animal
  • Gene Expression
  • Gene Expression Regulation, Neoplastic
  • Glioma / genetics*
  • Glioma / metabolism
  • Glioma / mortality
  • Glioma / pathology
  • Humans
  • Immunohistochemistry
  • MEF2 Transcription Factors / genetics*
  • MEF2 Transcription Factors / metabolism
  • Male
  • Mice
  • Neoplasm Grading
  • Prognosis

Substances

  • MEF2 Transcription Factors