ArticlePloS one2014
Targeting class IA PI3K isoforms selectively impairs cell growth, survival, and migration in glioblastoma.
Article in PloS one, 2014. 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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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
26 citing papers in PubMed, 41 citations in OpenAlex.
- Duvelisib with Docetaxel for Patients with Anti-PD-1 Refractory, Recurrent, or Metastatic Head and Neck Squamous Cell Carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Trial
- Glioblastoma multiforme: insights into pathogenesis, key signaling pathways, and therapeutic strategies.Molecular cancer · 2025Review
- Selective regulation of chemosensitivity in glioblastoma by phosphatidylinositol 3-kinase beta.iScience · 2024Article
- Signaling pathways and therapeutic approaches in glioblastoma multiforme (Review).International journal of oncology · 2022Review
- Polyunsaturated Fatty Acid-Enriched Lipid Fingerprint of Glioblastoma Proliferative Regions Is Differentially Regulated According to Glioblastoma Molecular Subtype.International journal of molecular sciences · 2022Article
- LncRNA LINC00460 facilitates the proliferation and metastasis of renal cell carcinoma via PI3K/AKT signaling pathway.Journal of Cancer · 2022Article
- Clinicopathological and genomic features in patients with head and neck neuroendocrine carcinoma.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021Article
- Pancreatic cancer intrinsic PI3Kα activity accelerates metastasis and rewires macrophage component.EMBO molecular medicine · 2021Article
- Combined PI3Kα-mTOR Targeting of Glioma Stem Cells.Scientific reports · 2020Article
- Role of PI3K/AKT pathway in cancer: the framework of malignant behavior.Molecular biology reports · 2020Review
- Gene Expression Signatures Identify Novel Therapeutics for Metastatic Pancreatic Neuroendocrine Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- The PI3K subunits, P110α and P110β are potential targets for overcoming P-gp and BCRP-mediated MDR in cancer.Molecular cancer · 2020Article
- Nicotine promotes the development of non-small cell lung cancer through activating LINC00460 and PI3K/Akt signaling.Bioscience reports · 2019Article
- PI3K Signaling in Neurons: A Central Node for the Control of Multiple Functions.International journal of molecular sciences · 2018Review
- Review
- PIK3CB/p110β is a selective survival factor for glioblastoma.Neuro-oncology · 2018Article
- Recent advances in the use of PI3K inhibitors for glioblastoma multiforme: current preclinical and clinical development.Molecular cancer · 2017Review
- CMV70-3P miRNA contributes to the CMV mediated glioma stemness and represents a target for glioma experimental therapy.Oncotarget · 2017Article
- The Role of Class IA Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunits in Glioblastoma.Frontiers in oncology · 2017Review
- Targeting of glioblastoma cell lines and glioma stem cells by combined PIM kinase and PI3K-p110α inhibition.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway is frequently activated in human cancer and plays a crucial role in glioblastoma biology. We were interested in gaining further insight into the potential of targeting PI3K isoforms as a novel anti-tumor approach in glioblastoma. Consistent expression of the PI3K catalytic isoform PI3K p110α was detected in a panel of glioblastoma patient samples. In contrast, PI3K p110β expression was only rarely detected in glioblastoma patient samples. The expression of a module comprising the epidermal growth factor receptor (EGFR)/PI3K p110α/phosphorylated ribosomal S6 protein (p-S6) was correlated with shorter patient survival. Inhibition of PI3K p110α activity impaired the anchorage-dependent growth of glioblastoma cells and induced tumor regression in vivo. Inhibition of PI3K p110α or PI3K p110β also led to impaired anchorage-independent growth, a decreased migratory capacity of glioblastoma cells, and reduced the activation of the Akt/mTOR pathway. These effects were selective, because targeting of PI3K p110δ did not result in a comparable impairment of glioblastoma tumorigenic properties. Together, our data reveal that drugs targeting PI3K p110α can reduce growth in a subset of glioblastoma tumors characterized by the expression of EGFR/PI3K p110α/p-S6.
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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.