ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Myocyte enhancer factor 2D promotes tumorigenicity in malignant glioma cells.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- DNA methylation remodeling in temozolomide resistant recurrent glioblastoma: comparing epigenetic dynamics in vitro and in vivo.Journal of translational medicine · 2025Article
- MEF2D Functions as a Tumor Suppressor in Breast Cancer.International journal of molecular sciences · 2024Article
- The Molecular and Biological Function of MEF2D in Leukemia.Advances in experimental medicine and biology · 2024Review
- MEF-2 isoforms' (A-D) roles in development and tumorigenesis.Oncotarget · 2019Review
- Molecular imaging HDACs class IIa expression-activity and pharmacologic inhibition in intracerebral glioma models in rats using PET/CT/(MRI) with [Scientific reports · 2019Article
- Long noncoding RNA DLEU1 aggravates glioma progression via the miR-421/MEF2D axis.OncoTargets and therapy · 2019Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
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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.
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