ArticleCancer cell2013
Gain of interaction with IRS1 by p110α-helical domain mutants is crucial for their oncogenic functions.
Article in Cancer cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 121 citations in OpenAlex.
- Correlation between PIK3CA mutations in cell-free DNA and everolimus efficacy in HRBritish journal of cancer · 2017Trial
- Protein-protein interactions as therapeutic targets in breast cancer: integrated computational and experimental advances, mechanisms and clinical translation.Molecular biology reports · 2026Review
- IRS4 is a PI3K-activating cancer dependency up-regulated through DNA rearrangements or epigenetic mechanisms in multiple solid tumors.Science advances · 2026Article
- Pan-cancer inference and validation of hypermorphic, hypomorphic and neomorphic mutations.Nature genetics · 2026Article
- Decoding the functional impact of the cancer genome through protein-protein interactions.Nature reviews. Cancer · 2025Review
- Oncogenic activation ofGenes & diseases · 2025Review
- Leucine-Rich Alpha-2-Glycoprotein 1 Promotes Metastatic Colorectal Cancer Growth Through Human Epidermal Growth Factor Receptor 3 Signaling.Gastroenterology · 2025Article
- Targeting PI3K family with small-molecule inhibitors in cancer therapy: current clinical status and future directions.Molecular cancer · 2024Review
- Arachidonic acid released by PIK3CA mutant tumor cells triggers malignant transformation of colonic epithelium by inducing chromatin remodeling.Cell reports. Medicine · 2024Article
- Targeting the SOX2/CDP protein complex with a peptide suppresses the malignant progression of esophageal squamous cell carcinoma.Cell death discovery · 2023Article
- Phosphorylation at tyrosine 317 and 508 are crucial for PIK3CA/p110α to promote CRC tumorigenesis.Cell & bioscience · 2023Article
- Structural and mechanistic insights provided by single particle cryo-EM analysis of phosphoinositide 3-kinase (PI3Kα).Biochimica et biophysica acta. Reviews on cancer · 2023Review
- PD-L1 expression is regulated by ATP-binding of the ERBB3 pseudokinase domain.Genes & diseases · 2023Article
- ERK1/2 inhibitors act as monovalent degraders inducing ubiquitylation and proteasome-dependent turnover of ERK2, but not ERK1.The Biochemical journal · 2023Article
- Targeting p85β nuclear translocation for the tumors withGenes & diseases · 2022Article
- Integrated cohort of esophageal squamous cell cancer reveals genomic features underlying clinical characteristics.Nature communications · 2022Article
- PIK3CA mutations-mediated downregulation of circLHFPL2 inhibits colorectal cancer progression via upregulating PTEN.Molecular cancer · 2022Article
- Nuclear translocation of p85β promotes tumorigenesis of PIK3CA helical domain mutant cancer.Nature communications · 2022Article
- The 'New (Nu)-clear' evidence for the tumor-driving role of PI3K.Acta materia medica · 2022Article
- The Role of mTOR Signaling as a Therapeutic Target in Cancer.International journal of molecular sciences · 2021Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
Abstract
PIK3CA, which encodes the p110α catalytic subunit of phosphatidylinositol 3-kinase α, is frequently mutated in human cancers. Most of these mutations occur at two hot-spots: E545K and H1047R located in the helical domain and the kinase domain, respectively. Here, we report that p110α E545K, but not p110α H1047R, gains the ability to associate with IRS1 independent of the p85 regulatory subunit, thereby rewiring this oncogenic signaling pathway. Disruption of the IRS1-p110α E545K interaction destabilizes the p110α protein, reduces AKT phosphorylation, and slows xenograft tumor growth of a cancer cell line expressing p110α E545K. Moreover, a hydrocarbon-stapled peptide that disrupts this interaction inhibits the growth of tumors expressing p110α E545K.
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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.