ArticleOncogene2009
The pyridinylfuranopyrimidine inhibitor, PI-103, chemosensitizes glioblastoma cells for apoptosis by inhibiting DNA repair.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 78 citations in OpenAlex.
- Single-Cell Multiomic Profiling Uncovers Radiation Dosage-Sensitive, Cluster-Specific Regulatory Dynamics in Glioblastoma.bioRxiv : the preprint server for biology · 2025Article
- Neuroprotection against beta-amyloid toxicity by the novel estrogen receptor modulator STX requires convergent signaling pathways.Frontiers in molecular neuroscience · 2025Article
- Systematic pan-cancer analysis identifies ZBTB11 as a potential pan-cancer biomarker and immunotherapy target in multiple tumor types.Discover oncology · 2024Article
- Identification of Cuproptosis-Related Genes for Molecular Subtyping: Predicting Prognostic and Therapeutic Response in Glioma.OncoTargets and therapy · 2024Article
- Unveiling Novel Avenues in mTOR-Targeted Therapeutics: Advancements in Glioblastoma Treatment.International journal of molecular sciences · 2023Review
- Artificial intelligence to guide precision anticancer therapy with multitargeted kinase inhibitors.BMC cancer · 2022Article
- The DNA Double-Strand Break Repair in Glioma: Molecular Players and Therapeutic Strategies.Molecular neurobiology · 2022Review
- Development and Evolution of DNA-Dependent Protein Kinase Inhibitors toward Cancer Therapy.International journal of molecular sciences · 2022Review
- PI3K Inhibitors in Cancer: Clinical Implications and Adverse Effects.International journal of molecular sciences · 2021Review
- Targeting the lysosome by an aminomethylated Riccardin D triggers DNA damage through cathepsin B-mediated degradation of BRCA1.Journal of cellular and molecular medicine · 2019Article
- Inhibition of PI3K signalling increases the efficiency of radiotherapy in glioblastoma cells.International journal of oncology · 2018Article
- Inhibition of the PI3K but not the MEK/ERK pathway sensitizes human glioma cells to alkylating drugs.Cancer cell international · 2018Article
- The effects of PI3K-mediated signalling on glioblastoma cell behaviour.Oncogenesis · 2017Article
- Review
- The Role of Class IA Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunits in Glioblastoma.Frontiers in oncology · 2017Review
- Dual targeting of PI3K and MEK enhances the radiation response of K-RAS mutated non-small cell lung cancer.Oncotarget · 2016Article
- Dual PI-3 kinase/mTOR inhibition impairs autophagy flux and induces cell death independent of apoptosis and necroptosis.Oncotarget · 2016Article
- Hypoxia on the Expression of Hepatoma Upregulated Protein in Prostate Cancer Cells.Frontiers in oncology · 2016Article
- Judicious Toggling of mTOR Activity to Combat Insulin Resistance and Cancer: Current Evidence and Perspectives.Frontiers in pharmacology · 2016Review
- Effects of oxygen on the antigenic landscape of prostate cancer cells.BMC research notes · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The failure of conventional therapies in glioblastoma (GBM) is largely due to an aberrant activity of survival cascades, such as PI3 kinase (PI3K)/Akt-mediated signaling. This study is the first to show that the class I PI3K inhibitor, PI-103, enhances chemotherapy-induced cell death of GBM cells. Concurrent treatment with PI-103 and DNA-damaging drugs, in particular doxorubicin, significantly increases apoptosis and reduces colony formation compared with chemotherapy treatment alone. The underlying molecular mechanism for this chemosensitization was shown by two independent approaches, that is, pharmacological and genetic inhibition of PI3K, DNA-PK and mTOR, to involve inhibition of DNA-PK-mediated DNA repair. Accordingly, blockage of PI3K or DNA-PK, but not of mTOR, significantly delays the resolution of doxorubicin-induced DNA damage and concomitantly increases apoptosis. Importantly, not only are several GBM cell lines chemosensitized by PI-103 but also GBM stem cells. Clinical relevance was further confirmed by the use of primary cultured GBM cells, which also exhibit increased cell death and reduced colony formation on combined treatment with PI-103 and doxorubicin. By identifying class I PI3K inhibitors as powerful agents in enhancing the lethality of DNA-damaging drugs, to which GBMs are usually considered unresponsive, our findings have important implications for the design of rational combination regimens in overcoming the frequent chemoresistance of GBM.
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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 OpenQuestion graph.