DLC2 inhibits development of glioma through regulating the expression ratio of TAp73α/TAp73β

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Chao Cheng1, Suyin Feng1, Jiantong Jiao1

  • 1Department of Neurosurgery, Wuxi People's Hospital of Nanjing Medical University Wuxi 214023, Jiangsu, China.

American Journal of Cancer Research
|August 11, 2018
PubMed

Insights

Deleted in liver cancer 2 (DLC2) inhibits glioma development by targeting TAp73α for degradation. This mechanism reduces the TAp73α/TAp73β ratio, impacting glioma cell proliferation and apoptosis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Gliomas exhibit high TAp73α expression and TAp73α/TAp73β ratios, with opposing roles in cell proliferation and apoptosis.
  • Deleted in liver cancer 2 (DLC2) is downregulated in gliomas, inversely correlating with TAp73α levels and the TAp73α/TAp73β ratio.

Purpose of the Study:

  • To elucidate the anti-tumor mechanism of DLC2 in glioma.
  • To investigate the role of DLC2 in regulating TAp73α and TAp73β expression in glioma cells.

Main Methods:

  • Analysis of TAp73α and TAp73β expression and their ratio in gliomas.
  • Investigation of DLC2 expression and its correlation with TAp73α/TAp73β ratio.
  • Assessment of DLC2's effect on glioma cell proliferation and apoptosis.
  • Examination of DLC2-TAp73α interaction and ubiquitination via SAM domain.

Main Results:

  • DLC2 inhibits glioma development by decreasing TAp73α expression, altering the TAp73α/TAp73β ratio.
  • DLC2 directly interacts with TAp73α, inducing its ubiquitination and degradation, a process mediated by the SAM domain of DLC2.
  • Deletion of the SAM domain in DLC2 abrogates TAp73α interaction and degradation, diminishing DLC2's tumor-suppressive effect.

Conclusions:

  • DLC2 functions as a tumor suppressor in gliomas by targeting TAp73α for degradation.
  • The DLC2-mediated reduction in TAp73α levels and subsequent alteration of the TAp73α/TAp73β ratio represent a key anti-glioma mechanism.
Keywords:
DLC2Gliomaapoptosisp73proliferation

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