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Published on: February 3, 2017
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.
Background:
Tripartite motif-containing protein 28 (TRIM28) is a transcriptional corepressor involved in the regulation of several cancers, including glioma. It has been reported that TRIM28 takes part in the process of autophagy. However, its effect on the autophagy and cell proliferation in gliomas has not been elucidated. Here, we report a novel tumor cell proliferation mechanism in which TRIM28-regulated autophagy promotes glioma tumor cell proliferation.
Materials And Methods:
We analyzed the expressions of TRIM28 and LC3 in different WHO grades of gliomas by IHC assays. We then knocked down and overexpressed TRIM28 or knocked down ATG5 in U251 cells and confirmed its roles in autophagy and cell proliferation via cell counting, immunofluorescence, and Western blot.
Results:
The results showed that TRIM28 and autophagy levels were significantly increased with the progression of tumor grade in glioma. TRIM28 promoted glioblastoma cell proliferation. Knockdown of TRIM28 inhibited autophagy in glioblastoma cells. Meanwhile, TRIM28 promoted glioblastoma cell proliferation by modulating TRIM28.
Conclusion:
These data demonstrated that TRIM28 activates autophagy and increases cell proliferation in glioma.
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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