ArticleMolecular medicine (Cambridge, Mass.)2019
Inhibition of phosphatidylinositol 3-kinase by PX-866 suppresses temozolomide-induced autophagy and promotes apoptosis in glioblastoma cells.
Article in Molecular medicine (Cambridge, Mass.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Article
- Corrigendum to: Cellular and in vivo activity of a novel PI3K inhibitor, PX-866, against human glioblastoma.Neuro-oncology · 2026Article
- Inhibition of FOS-Like Antigen 1 Reduces Chemoresistance to Temozolomide Through Stemness Reprogramming via IL-6/STAT3MedComm · 2026Article
- Review
- Crosstalk between metabolism and cell death in tumorigenesis.Molecular cancer · 2024Review
- Inhibitors of phosphoinositide 3-kinase (PI3K) and phosphoinositide 3-kinase-related protein kinase family (PIKK).Journal of enzyme inhibition and medicinal chemistry · 2023Review
- Temozolomide and chloroquine co-loaded mesoporous silica nanoparticles are effective against glioma.Heliyon · 2023Article
- Macrophage's role in solid tumors: two edges of a sword.Cancer cell international · 2023Article
- The Glioblastoma Landscape: Hallmarks of Disease, Therapeutic Resistance, and Treatment Opportunities.Medical research archives · 2023Article
- The PYK2 inhibitor PF-562271 enhances the effect of temozolomide on tumor growth in a C57Bl/6-Gl261 mouse glioma model.Journal of neuro-oncology · 2023Article
- Regulation of temozolomide resistance via lncRNAs: Clinical and biological properties of lncRNAs in gliomas (Review).International journal of oncology · 2022Review
- Abrogation of Cellular Senescence Induced by Temozolomide in Glioblastoma Cells: Search for Senolytics.Cells · 2022Article
- SOCS5 contributes to temozolomide resistance in glioblastoma by regulating Bcl-2-mediated autophagy.Bioengineered · 2022Article
- Biochanin A Sensitizes Glioblastoma to Temozolomide by Inhibiting Autophagy.Molecular neurobiology · 2022Article
- Bortezomib abrogates temozolomide-induced autophagic flux through an ATG5 dependent pathway.Frontiers in cell and developmental biology · 2022Article
- Sesquiterpene Lactones and Cancer: New Insight into Antitumor and Anti-inflammatory Effects of Parthenolide-Derived Dimethylaminomicheliolide and Micheliolide.Computational and mathematical methods in medicine · 2022Review
- Advances in Immunosuppressive Agents Based on Signal Pathway.Frontiers in pharmacology · 2022Review
- Targeting Autophagy with Natural Products as a Potential Therapeutic Approach for Cancer.International journal of molecular sciences · 2021Review
- Review
- Involvement of PI3K Pathway in Glioma Cell Resistance to Temozolomide Treatment.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundTemozolomide (TMZ) is the most commonly used chemotherapeutic agent used to treat glioblastoma (GBM), which causes significant DNA damage to highly proliferative cells. Our observations have added to accumulating evidence that TMZ induces stress-responsive cellular programs known to promote cell survival, including autophagy. As such, targeting these survival pathways may represent new vulnerabilities of GBM after treatment with TMZ.
methodsUsing the T98G human glioma cell line, we assessed the molecular signaling associated with TMZ treatment, the cellular consequences of using the pan-PI3K inhibitor PX-866, and performed clonogenic assays to determine the effect sequential treatment of TMZ and PX-866 had on colony formation. Additionally, we also use subcutaneous GBM patient derived xenograft (PDX) tumors to show relative LC3 protein expression and correlations between survival pathways and molecular markers which dictate clinical responsiveness to TMZ.
resultsHere, we report that TMZ can induce autophagic flux in T98G glioma cells. GBM patient-derived xenograft (PDX) tumors treated with TMZ also display an increase in the autophagosome marker LC3 II. Additionally, O
conclusionsThe understanding of how TMZ induces survival pathways, such as autophagy, may offer new therapeutic vulnerabilities and opportunities to use sequential inhibition of alternate pro-survival pathways that regulate autophagy. As such, identification of additional ways to inhibit TMZ-induced autophagy could enhance the efficacy of TMZ.
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