ArticleScientific reports2025
TLK1 as a therapeutic target in TMZ resistant glioblastoma using small molecule inhibitor.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Rewiring mitotic checkpoint control via Mps1 inhibition overcomes DNA repair-mediated resistance in glioblastoma.The Journal of biological chemistry · 2026Article
- Stem-like characteristics across sequentially temozolomide-adapted glioblastoma cell populations with increasing levels of acquired resistance.Molecular biology reports · 2026Article
- Meningeal immunity and "Interstitial" therapy: a new paradigm for immunotherapy in glioblastoma.Frontiers in immunology · 2026Review
- XPO1-inhibitor Selinexor induces MGMT expression by activating PKA-CREB signaling inFrontiers in oncology · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The acquired resistance to existing therapies poses a grave concern in achieving successful therapeutic outcomes. Temozolomide (TMZ), a widely used alkylating chemotherapeutic in Glioblastoma therapy, often encounters resistance, necessitating the investigation of the underlying mechanisms of TMZ-acquired resistance. To study TMZ resistance, a cell-based model system was generated by intermittently exposing glioblastoma cells to increasing concentrations and time of TMZ over six months. The survival response of cells at higher concentrations confirmed TMZ-resistant cells, which exhibited a phenotypic shift toward a mesenchymal-like state, with decreased epithelial traits, indicating mesenchymal-epithelial transition (MET). This transition likely facilitates the stabilization and clonal growth of TMZ-resistant cells. Subsequent analysis revealed elevated expression of TLK1, a DNA repair protein, thus reinforcing its potential involvement in mechanisms associated with acquired resistance. To explore the therapeutic aspect of TLK1 inhibition, we utilized an in-house developed TLK1 inhibitor, J54. The inhibition of TLK1 in TMZ-resistant cells enhanced cytotoxicity, indicating TLK1 as a potential target to combat TMZ resistance. Moreover, TLK1 inhibition reduced cell migration and invasion, implying its role in promoting metastasis. In conclusion, our study sheds light on the role of TLK1 in the context of TMZ resistance, highlighting its potential as a valuable target for therapeutic intervention.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.