TRIM28 activates autophagy and promotes cell proliferation in glioblastoma

Yong Peng1, Mingming Zhang1, Zhongzhong Jiang1

  • 1Department of Neurosurgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China, foxpy195@csu.edu.cn.

Oncotargets and Therapy
|January 19, 2019
PubMed
Abstract

Insights

Tripartite motif-containing protein 28 (TRIM28) activates autophagy, promoting glioma cell proliferation. Inhibiting TRIM28 reduces autophagy and glioblastoma cell growth, revealing a novel therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cellular Biology

Background:

  • Tripartite motif-containing protein 28 (TRIM28) is a transcriptional corepressor implicated in glioma regulation.
  • TRIM28's role in autophagy and its specific impact on glioma cell proliferation remain unclear.

Purpose of the Study:

  • To elucidate the mechanism by which TRIM28 influences autophagy and cell proliferation in glioma.
  • To investigate TRIM28 as a potential therapeutic target in glioma treatment.

Main Methods:

  • Immunohistochemistry (IHC) assays to analyze TRIM28 and LC3 expression in gliomas.
  • Gene manipulation (knockdown/overexpression) of TRIM28 and ATG5 in U251 cells.
  • Assessment of autophagy and cell proliferation using cell counting, immunofluorescence, and Western blot.

Main Results:

  • TRIM28 and autophagy levels significantly correlate with glioma WHO tumor grade progression.
  • TRIM28 overexpression enhances glioblastoma cell proliferation, while TRIM28 knockdown inhibits it.
  • TRIM28 knockdown leads to decreased autophagy in glioblastoma cells.

Conclusions:

  • TRIM28 acts as an activator of autophagy in glioma.
  • TRIM28 significantly contributes to glioma cell proliferation through autophagy modulation.

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