ArticleNeuro-oncology2018
PIK3CB/p110β is a selective survival factor for glioblastoma.
Article in Neuro-oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed.
- PI3K/AKT signaling pathway: molecular crossroads in tumorigenesis and therapeutic innovation.Signal transduction and targeted therapy · 2026Review
- PIK3CA mutations and PI3K isoform expression define prognostic signatures in ovarian clear cell carcinoma.Archives of gynecology and obstetrics · 2026Article
- Multi-Omics and Machine Learning Analyses Reveal PIK3CG, PRKCD, and TRIM22 as Potential Markers of Poor Prognosis and Immune Activation in Glioblastoma.Journal of Korean medical science · 2026Article
- The role of genes related to excitotoxicity in glioma prognosis.Discover oncology · 2025Article
- Targeting the proliferation of glioblastoma cells and enhancement of doxorubicin and temozolomide cytotoxicity through inhibition of PFKFB4 and HMOX1 genes with siRNAs.Scientific reports · 2025Article
- PI3Kβ moonlights as a protein kinase: driving fatty acid metabolism and histone acetylation in cancer.Cancer biology & medicine · 2025Article
- Targeting PIK3CB/YAP1 improves the sensitivity of paclitaxel by suppressing aging in head and neck squamous tumor cells.Cancer cell international · 2025Article
- USP8-mediated PTK7 promotes PIK3CB-related pathway to accelerate the malignant progression of non-small cell lung cancer.Thoracic cancer · 2025Article
- Role and Therapeutic Potential of miR-301b-3p in Regulating the PI3K-AKT Pathway via PIK3CB in Eosinophilic Chronic Rhinosinusitis.Journal of inflammation research · 2025Article
- Targeting the PI3K/AKT/mTOR pathway in lung cancer: mechanisms and therapeutic targeting.Frontiers in pharmacology · 2025Review
- Molecular Basis of Oncogenic PI3K Proteins.Cancers · 2024Review
- Selective regulation of chemosensitivity in glioblastoma by phosphatidylinositol 3-kinase beta.iScience · 2024Article
- Sanguinarine inhibits melanoma invasion and migration by targeting the FAK/PI3K/AKT/mTOR signalling pathway.Pharmaceutical biology · 2023Article
- From signalling pathways to targeted therapies: unravelling glioblastoma's secrets and harnessing two decades of progress.Signal transduction and targeted therapy · 2023Review
- Exosomal PIK3CB promotes PD-L1 expression and malignant transformation in esophageal squamous cell carcinoma.Medical oncology (Northwood, London, England) · 2023Article
- The Glioblastoma Landscape: Hallmarks of Disease, Therapeutic Resistance, and Treatment Opportunities.Medical research archives · 2023Article
- Development and safety of PI3K inhibitors in cancer.Archives of toxicology · 2023Review
- Nucleic acid drug vectors for diagnosis and treatment of brain diseases.Signal transduction and targeted therapy · 2023Review
- Article
- Leukocytes mediate disease pathogenesis in the Ndufs4(KO) mouse model of Leigh syndrome.JCI insight · 2022Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Glioblastoma (GBM) is difficult to treat. Phosphoinositide 3-kinase (PI3K) is an attractive therapeutic target for GBM; however, targeting this pathway to effectively treat GBM is not successful because the roles of PI3K isoforms remain to be defined. The aim of this study is to determine whether PIK3CB/p110β, but not other PI3K isoforms, is a biomarker for GBM recurrence and important for cell survival. Methods: Gene expression and clinical relevance of PI3K genes in GBM patients were analyzed using online databases. Expression/activity of PI3K isoforms was determined using immunoblotting. PI3K genes were inhibited using short hairpin RNAs or isoform-selective inhibitors. Cell viability/growth was assessed by the MTS assay and trypan blue exclusion assay. Apoptosis was monitored using the caspase activity assay. Mouse GBM xenograft models were used to gauge drug efficacy. Results: PIK3CB/p110β was the only PI3K catalytic isoform that significantly correlated with high incidence rate, risk, and poor survival of recurrent GBM. PIK3CA/p110α, PIK3CB/p110β, and PIK3CD/p110δ were differentially expressed in GBM cell lines and primary tumor cells derived from patient specimens, whereas PIK3CG/p110γ was barely detected. PIK3CB/p110β protein levels presented a stronger association with the activities of PI3K signaling than other PI3K isoforms. Blocking p110β deactivated PI3K signaling, whereas inhibition of other PI3K isoforms had no effect. Specific inhibitors of PIK3CB/p110β, but not other PI3K isoforms, remarkably suppressed viability and growth of GBM cells and xenograft tumors in mice, with minimal cytotoxic effects on astrocytes. Conclusions: PIK3CB/p110β is a biomarker for GBM recurrence and selectively important for GBM cell survival.
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