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TRIM22 promotes glioblastoma development by ubiquitinating Bcl-2
Jiahao Zhang1, Yuning Chen1, Gaosong Wang1
1Department of Neurosurgery, Wuxi People's Hospital Affiliated with Nanjing Medical University, Wuxi, Jiangsu, China.
Molecular & Cellular Oncology
|June 24, 2025
Summary
Elevated TRIM22 expression drives glioblastoma (GBM) progression. Inhibiting TRIM22 promotes GBM cell apoptosis and may offer a new target for glioma immunotherapy.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Glioblastoma (GBM) shows increased TRIM22 expression linked to tumor advancement.
- TRIM22's role in GBM pathogenesis requires further elucidation.
Purpose of the Study:
- To investigate the functional role of TRIM22 in glioblastoma.
- To explore the molecular mechanisms by which TRIM22 influences GBM cell proliferation and apoptosis.
- To assess TRIM22 as a potential therapeutic target for glioma.
Main Methods:
- Analysis of TRIM22 expression in TCGA/GEO databases.
- Cellular assays to evaluate the effects of TRIM22 knockdown and overexpression on GBM cells.
- Ubiquitination microarray to identify TRIM22 interacting proteins.
- Flow cytometry (FCM) for apoptosis analysis.
- Western blot to assess protein expression levels (Bcl-2).
- Immunoprecipitation (IP) and ubiquitination assays to confirm TRIM22-Bcl-2 interaction and ubiquitination.
Main Results:
- TRIM22 overexpression correlates with glioma progression; TRIM22 deficiency inhibits GBM cell proliferation.
- TRIM22 knockdown significantly promotes GBM cell apoptosis.
- TRIM22 was identified as an activator of Bcl-2, increasing its protein stability via nondegradative ubiquitination.
- TRIM22 directly binds to Bcl-2, suggesting a regulatory relationship.
Conclusions:
- TRIM22 plays a significant role in glioma progression by modulating Bcl-2 stability and function.
- TRIM22 inhibition promotes apoptosis in glioblastoma cells.
- TRIM22 represents a promising novel therapeutic target for glioma immunotherapy, potentially enhancing treatment sensitivity.
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