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Repression of Dok7 expression mediated by DNMT1 promotes glioma cells proliferation

Cheng-Dao Hua1, Er-Bao Bian1, Er-Feng Chen1

  • 1Department of Neurosurgery, The Second Affiliated Hospital of Anhui Medical University, Hefei, 230601, China; Cerebral Vascular Disease Research Center, Anhui Medical University, Hefei, 230601, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|July 11, 2018
PubMed

Insights

Dok7 expression is reduced in malignant glioma, and its restoration inhibits tumor growth. Epigenetic silencing of Dok7 may offer a new therapeutic strategy for glioma.

Area of Science:

  • Neuro-oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Malignant glioma is a common primary central nervous system tumor.
  • Molecular mechanisms driving glioma progression are not fully understood.

Purpose of the Study:

  • To investigate the role of Dok7 in glioma development.
  • To explore Dok7's potential as a therapeutic target.

Main Methods:

  • Analyzed Dok7 expression in human glioma tissues.
  • Overexpressed Dok7 in glioma cells in vitro and in vivo.
  • Utilized 5-Aza-2'-deoxycytidine (5-Aza), a DNA methylation inhibitor.
  • Performed DNMT1 knockdown experiments.

Main Results:

  • Dok7 expression was downregulated in human glioma tissues.
  • Dok7 overexpression suppressed glioma cell proliferation, colony formation, and tumor growth in vivo.
  • 5-Aza treatment reduced Dok7 promoter hypermethylation and restored Dok7 expression.
  • DNMT1 knockdown led to Dok7 promoter demethylation and increased Dok7 expression.

Conclusions:

  • Epigenetic silencing of Dok7 contributes to glioma development.
  • Restoring Dok7 expression via epigenetic modulation is a potential therapeutic strategy for glioma.
Keywords:
5-AzaDNMT1Dok7Glioma

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