ArticleNeuro-oncology2011
Identification of novel synergistic targets for rational drug combinations with PI3 kinase inhibitors using siRNA synthetic lethality screening against GBM.
Article in Neuro-oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 47 citations in OpenAlex.
- Corrigendum to: Cellular and in vivo activity of a novel PI3K inhibitor, PX-866, against human glioblastoma.Neuro-oncology · 2026Article
- Integrative bioinformatic analysis to identify potential phytochemical candidates for glioblastoma.Heliyon · 2024Article
- Crucial Roles of miR-625 in Human Cancer.Frontiers in medicine · 2022Review
- Super-enhancer-associated TMEM44-AS1 aggravated glioma progression by forming a positive feedback loop with Myc.Journal of experimental & clinical cancer research : CR · 2021Article
- Prediction and analysis of hub genes between glioblastoma and low-grade glioma using bioinformatics analysis.Medicine · 2021Article
- Bioinformatic gene analysis for potential therapeutic targets of Huntington's disease in pre-symptomatic and symptomatic stage.Journal of translational medicine · 2020Article
- Combined elevation of TRIB2 and MAP3K1 indicates poor prognosis and chemoresistance to temozolomide in glioblastoma.CNS neuroscience & therapeutics · 2020Article
- Article
- Current Challenges and Opportunities in Treating Glioblastoma.Pharmacological reviews · 2018Article
- Targeting dual specificity protein kinase TTK attenuates tumorigenesis of glioblastoma.Oncotarget · 2018Article
- Glioma: experimental models and reality.Acta neuropathologica · 2017Review
- The Identification of Key Genes and Pathways in Glioma by Bioinformatics Analysis.Journal of immunology research · 2017Article
- MicroRNA-625 inhibits the proliferation and increases the chemosensitivity of glioma by directly targeting AKT2.American journal of cancer research · 2017Article
- Network modeling of kinase inhibitor polypharmacology reveals pathways targeted in chemical screens.PloS one · 2017Article
- Contemporary murine models in preclinical astrocytoma drug development.Neuro-oncology · 2015Review
- Evolutionarily conserved genetic interactions with budding and fission yeast MutS identify orthologous relationships in mismatch repair-deficient cancer cells.Genome medicine · 2014Article
- Differential microRNA expression signatures and cell type-specific association with Taxol resistance in ovarian cancer cells.Drug design, development and therapy · 2014Article
- MicroRNA-26a promotes tumor growth and angiogenesis in glioma by directly targeting prohibitin.CNS neuroscience & therapeutics · 2013Article
- A kinome-wide RNAi screen in Drosophila Glia reveals that the RIO kinases mediate cell proliferation and survival through TORC2-Akt signaling in glioblastoma.PLoS genetics · 2013Article
- Signal transduction molecule patterns indicating potential glioblastoma therapy approaches.OncoTargets and therapy · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Several small molecules that inhibit the PI3 kinase (PI3K)-Akt signaling pathway are in clinical development. Although many of these molecules have been effective in preclinical models, it remains unclear whether this strategy alone will be sufficient to interrupt the molecular events initiated and maintained by signaling along the pathways because of the activation of other pathways that compensate for the inhibition of the targeted kinase. In this study, we performed a synthetic lethality screen to identify genes or pathways whose inactivation, in combination with the PI3K inhibitors PX-866 and NVPBEZ-235, might result in a lethal phenotype in glioblastoma multiforme (GBM) cells. We screened GBM cells (U87, U251, and T98G) with a large-scale, short hairpin RNA library (GeneNet), which contains 43 800 small interfering RNA sequences targeting 8500 well-characterized human genes. To decrease off-target effects, we selected overlapping genes among the 3 cell lines that synergized with PX-866 to induce cell death. To facilitate the identification of potential targets, we used a GSE4290 dataset and The Cancer Genome Atlas GBM dataset, identifying 15 target genes overexpressed in GBM tissues. We further analyzed the selected genes using Ingenuity Pathway Analysis software and showed that the 15 genes were closely related to cancer-promoting pathways, and a highly interconnected network of aberrations along the MYC, P38MAPK, and ERK signaling pathways were identified. Our findings suggest that inhibition of these pathways might increase tumor sensitivity to PX-866 and therefore represent a potential clinical therapeutic strategy.
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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.