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Unveiling the role of TAGLN2 in glioblastoma: From proneural-mesenchymal transition to Temozolomide resistance
TAGLN2’s role in aggressive brain tumors: linked to cell type changes and resistance to chemotherapy
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Abstract
TAGLN2 is prominently expressed in the mesenchymal subtype of glioblastoma, showing potential links to temozolomide resistance.
- TAGLN2 is involved in the transition from a proneural to a mesenchymal phenotype in glioblastoma, which is associated with resistance to temozolomide.
- Knocking down TAGLN2 can reduce cell proliferation and invasion, induce DNA damage and cell death, and increase sensitivity to temozolomide in glioblastoma cells.
- Increasing TAGLN2 levels enhances resistance to temozolomide in both cellular models and intracranial xenograft mouse models.
- TAGLN2 interacts with the ERK1/2 signaling pathway, with knockdown leading to decreased expression of activated ERK1/2 in the nucleus.
- The expression of the DNA repair protein MGMT is regulated by TAGLN2, linking it to temozolomide resistance mechanisms.
- NF-κB has been confirmed to regulate TAGLN2 expression, further implicating it in the pathways that promote mesenchymal transition and drug resistance.
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