ArticleBreast cancer research and treatment2019
Somatic loss of PIK3R1 may sensitize breast cancer to inhibitors of the MAPK pathway.
Article in Breast cancer research and treatment, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Cancer-AssociatedInternational journal of medical sciences · 2025Review
- Article
- Comparative genomic analysis of PIK3R1-mutated and wild-type breast cancers.Breast cancer research and treatment · 2024Article
- Integrative multi-omics characterization reveals sex differences in glioblastoma.Biology of sex differences · 2024Article
- Predictive, preventive, and personalized medicine in breast cancer: targeting the PI3K pathway.Journal of translational medicine · 2024Review
- Identification and comprehensive analysis of epithelial-mesenchymal transition related target genes of miR-222-3p in breast cancer.Frontiers in oncology · 2023Article
- Novel neoplasms associated with syndromic pediatric medulloblastoma: integrated pathway delineation for personalized therapy.Cell communication and signaling : CCS · 2022Article
- Targeted Sequencing of Taiwanese Breast Cancer with Risk Stratification by the Concurrent Genes Signature: A Feasibility Study.Journal of personalized medicine · 2021Article
- Patient-Specific Network for Personalized Breast Cancer Therapy with Multi-Omics Data.Entropy (Basel, Switzerland) · 2021Article
- Anthrax lethal factor cleaves regulatory subunits of phosphoinositide-3 kinase to contribute to toxin lethality.Nature microbiology · 2020Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe PI3K pathway, which includes the PI3K catalytic subunits p110α (PIK3CA) and the PI3K regulatory subunit p85α (PIK3R1), is the most frequently altered pathway in cancer. We encountered a breast cancer patient whose tumor contained a somatic alteration in PIK3R1. Some commercial sequencing platforms suggest that somatic mutations in PIK3R1 may sensitize cancers to drugs that inhibit the mammalian target of rapamycin (mTOR). However, a review of the preclinical and clinical literature did not find evidence substantiating that hypothesis. The purpose of this study was to knock out PIK3R1 in order to determine the optimal therapeutic approach for breast cancers lacking p85α.
methodsWe created an isogenic cellular system by knocking out both alleles of the PIK3R1 gene in the non-tumorigenic human breast cell line MCF-10A. Knockout cells were compared with wild-type cells by measuring growth, cellular signaling, and response to drugs.
resultsWe observed hyperphosphorylation of MEK in these knockouts, which sensitized PIK3R1-null cells to a MEK inhibitor, trametinib. However, they were not sensitized to the mTOR inhibitor, everolimus.
conclusionsOur findings suggest that breast cancers with loss of p85α may not respond to mTOR inhibition, but may be sensitive to MEK inhibition.
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