ArticleJournal of neuro-oncology2023
The PYK2 inhibitor PF-562271 enhances the effect of temozolomide on tumor growth in a C57Bl/6-Gl261 mouse glioma model.
Article in Journal of neuro-oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Dual targeting of interlocked PTK2B and MAPK signaling triggers synergistic ferroptosis via autophagic flux disruption in BRAFCell communication and signaling : CCS · 2026Article
- Window of opportunity study measuring defactinib and avutometinib delivery in glioblastomas.Cancer chemotherapy and pharmacology · 2026Article
- A patent review of cyclin-dependent kinase 5 (CDK5) inhibitors (1999-2025).Frontiers in bioengineering and biotechnology · 2026Review
- FAK modulates glioblastoma stem cell energetics via regulation of glycolysis and glutamine oxidation.Disease models & mechanisms · 2025Article
- Review
- A novel cuproptosis-associated LncRNA model predicting prognostic and immunotherapy response for glioma.Discover oncology · 2025Article
- Drug Combinations Targeting FAK and MEK Overcomes Tumor Heterogeneity in Glioblastoma.Pharmaceutics · 2025Article
- Pyk2/FAK Signaling Is Upregulated in Recurrent Glioblastoma Tumors in a C57BL/6/GL261 Glioma Implantation Model.International journal of molecular sciences · 2023Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe development of resistance to temozolomide (TMZ), a standard chemotherapeutic, limits the effective treatment of glioblastoma (GBM). Focal adhesion kinase (FAK) and proline rich tyrosine kinase 2 (Pyk2) regulate proliferation and invasion of GBM cells. We found that TMZ activates FAK and Pyk2 signaling in GBM. We hypothesized that pharmacological inhibitors of Pyk2/FAK together with TMZ can enhance the inhibitory effect of TMZ on tumor growth and dispersal and improve the treatment outcome.
methodsPrimary human GBM cell cultures and a C57Bl/6-GL261 mouse glioma implantation model were used. Pyk2 (Tyr579/580) and FAK (Tyr925) phosphorylation was analyzed by western blotting. Viability, cell cycle, migration, invasion and invadopodia formation were investigated in vitro. Animal survival, tumor size and invasion, TUNEL apoptotic cell death and the Ki67 proliferation index were evaluated in vivo upon treatment with TMZ (50 mg/kg, once/day, orally) and the Pyk2/FAK inhibitor PF-562271 (once/daily, 50 mg/kg, orally) vs. TMZ monotherapy.
resultsIn vitro studies revealed significantly reduced viability, cell cycle progression, invasion and invadopodia with TMZ (100 µM) + PF-562271 (16 nM) compared with TMZ alone. In vivo studies demonstrated that combinatorial treatment led to prominent reductions in tumor size and invasive margins, extensive signs of apoptosis and a reduced proliferation index, together with a 15% increase in the survival rate in animals, compared with TMZ monotherapy.
conclusionTMZ + PF-562271 eliminates TMZ-related Pyk2/FAK activation in GBM and improves the treatment efficacy.
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