ArticleCancer cell international2024
TUBB2B regulates epithelial-mesenchymal transition via interaction with Vimentin to promote glioma migration and invasion.
Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Focal astrocyte loss reveals nuclear translocation during lesion repopulation.Nature neuroscience · 2026Article
- Mitochondrial ribosomal protein MRPL27 supports glioma malignancy through regulation of oxidative phosphorylation.Cellular and molecular life sciences : CMLS · 2026Article
- SIRT5-RNF126 coordinated regulation of METTL17 stability controls mitochondrial function and glioma progression.Cell & bioscience · 2026Article
- Crebanine Protects HUVECs from LPS-Induced Inflammation and Oxidative Stress by Suppressing NF-κB Pathway.Biomolecules & therapeutics · 2026Article
- Application of the Mass Spectrometry-High-Throughput Technique Over the Immunohistochemical Analysis for Human Brain Tumor Diagnosis and Prognosis: Insights Into Biomarkers' Identification for the Case Study of Grade IV Astrocytomas and Meningiomas.Biomedical chromatography : BMC · 2025Article
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Authors and funding
12 authors.
Funding
Abstract
backgroundEpithelial-mesenchymal transition (EMT) plays a crucial role in the migration and invasion capabilities of glioblastoma (GBM) cells. Several studies have established tubulin as a significant regulator of the EMT process. Tubulin beta 2B class IIb (TUBB2B), a critical component of microtubules, has been linked to the prognosis of various tumors. However, the specific biological function and mechanism of TUBB2B in GBM remain unclear.
methodsIn vitro experiments demonstrated that TUBB2B knockdown inhibited the migration and invasion of GBM cells, while its overexpression enhanced these capabilities. Western blot, immunofluorescence (IF) and co-immunoprecipitation (Co-IP) assays revealed that TUBB2B interacts with Vimentin. Molecular docking and residue mutation scanning indicated that TUBB2B interacts with Vimentin at the R391/K392/A393/F394 sites. In vivo experiments using nude mice confirmed that TUBB2B knockdown inhibited GBM cell invasion and migration.
resultsTUBB2B was upregulated in GBM tissue samples compared with normal tissues. The sites of TUBB2B(R391/K392/A393/F394) physically interacts with Vimentin to induce EMT, which promotes migration and invasion.
conclusionTUBB2B may regulate EMT and promote the migration and invasion of GBM cells through its interaction with Vimentin, highlighting TUBB2B as a potential therapeutic target for GBM.
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