ArticleNature communications2022
Nuclear translocation of p85β promotes tumorigenesis of PIK3CA helical domain mutant cancer.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Predicting interaction-specific protein-protein interaction perturbations by missense variants with MutPred-PPI.bioRxiv : the preprint server for biology · 2026Article
- Phase separation of p85β modulates hepatocellular carcinoma progression through POLR1A.International journal of biological sciences · 2026Article
- The nuclear phosphoinositide-p53 signalosome in the regulation of cell motility.Protein & cell · 2025Review
- Depleting the Action of EZH2 through PI3K-mTOR Inhibition to Overcome Metastasis and Immunotherapy Resistance in Triple-Negative Breast Cancer.Molecular cancer therapeutics · 2025Article
- Targeting AQP5-mediated arginine deprivation in gastric cancer stem cells restores NK cell anti-tumor immunity.Cell reports. Medicine · 2025Article
- Double vulnerability of active-NRF2 lung squamous cell carcinoma to NRF2 and TRIM24.Molecular cancer · 2025Article
- ABCF1-K430-Lactylation promotes HCC malignant progression via transcriptional activation of HIF1 signaling pathway.Cell death and differentiation · 2025Article
- Oncogenic activation ofGenes & diseases · 2025Review
- p85β acts as a transcription cofactor and cooperates with BCLAF1 in the nucleus.Nature communications · 2025Article
- Molecular Basis of Oncogenic PI3K Proteins.Cancers · 2024Review
- Circulating exosomal PCAT1 as a complement of carcinoembryonic antigen for early colorectal cancer diagnosis.Heliyon · 2024Article
- Article
- Arachidonic acid released by PIK3CA mutant tumor cells triggers malignant transformation of colonic epithelium by inducing chromatin remodeling.Cell reports. Medicine · 2024Article
- Neutrophil extracellular traps induced by chemotherapy inhibit tumor growth in murine models of colorectal cancer.The Journal of clinical investigation · 2024Article
- Predictive, preventive, and personalized medicine in breast cancer: targeting the PI3K pathway.Journal of translational medicine · 2024Review
- The role of PIK3CA gene mutations in colorectal cancer and the selection of treatment strategies.Frontiers in pharmacology · 2024Review
- IL-13/IL-13RA2 signaling promotes colorectal cancer stem cell tumorigenesis by inducing ubiquitinated degradation of p53.Genes & diseases · 2024Article
- PD-L1 expression is regulated by ATP-binding of the ERBB3 pseudokinase domain.Genes & diseases · 2023Article
- Divergent roles of the regulatory subunits of class IA PI3K.Frontiers in endocrinology · 2023Review
- Targeting p85β nuclear translocation for the tumors withGenes & diseases · 2022Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
PI3Ks consist of p110 catalytic subunits and p85 regulatory subunits. PIK3CA, encoding p110α, is frequently mutated in human cancers. Most PIK3CA mutations are clustered in the helical domain or the kinase domain. Here, we report that p85β disassociates from p110α helical domain mutant protein and translocates into the nucleus through a nuclear localization sequence (NLS). Nuclear p85β recruits deubiquitinase USP7 to stabilize EZH1 and EZH2 and enhances H3K27 trimethylation. Knockout of p85β or p85β NLS mutant reduces the growth of tumors harboring a PIK3CA helical domain mutation. Our studies illuminate a novel mechanism by which PIK3CA helical domain mutations exert their oncogenic function. Finally, a combination of Alpelisib, a p110α-specific inhibitor, and an EZH inhibitor, Tazemetostat, induces regression of xenograft tumors harboring a PIK3CA helical domain mutation, but not tumors with either a WT PIK3CA or a PIK3CA kinase domain mutation, suggesting that the drug combination could be an effective therapeutic approach for PIK3CA helical domain mutant tumors.
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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 Socratic graph.