ArticleMolecular and cellular biology2008
Tyrosine phosphorylation of the nuclear receptor coactivator AIB1/SRC-3 is enhanced by Abl kinase and is required for its activity in cancer cells.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 61 citations in OpenAlex.
- Knowledge-driven interpretable neural networks provide mechanistic insight.Genome research · 2026Article
- The ULK1-NCOA3 axis restrains de novo lipogenesis and prevents diet-induced steatohepatitis and fibrosis in mice.The Journal of clinical investigation · 2026Article
- Phosphorylated NCOA6 promotes aggressiveness and contributes patient outcomes in estrogen receptor-positive breast cancer.Cancer cell international · 2025Article
- p160 nuclear receptor coactivator family members and their role in rare fusion‑driven neoplasms (Review).Oncology letters · 2024Review
- AIB1/SRC-3/NCOA3 function in estrogen receptor alpha positive breast cancer.Frontiers in endocrinology · 2023Review
- Patient-derived xenografts and in vitro model show rationale for imatinib mesylate repurposing in HEY1-NCoA2-driven mesenchymal chondrosarcoma.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Article
- SRC-3, a Steroid Receptor Coactivator: Implication in Cancer.International journal of molecular sciences · 2021Review
- The Role of Steroid Receptor Coactivators in Hormone Dependent Cancers and Their Potential as Therapeutic Targets.Hormones & cancer · 2016Review
- Amplified in Breast Cancer Regulates Transcription and Translation in Breast Cancer Cells.Neoplasia (New York, N.Y.) · 2016Article
- Characterization of a Steroid Receptor Coactivator Small Molecule Stimulator that Overstimulates Cancer Cells and Leads to Cell Stress and Death.Cancer cell · 2015Article
- Insights into Orphan Nuclear Receptors as Prognostic Markers and Novel Therapeutic Targets for Breast Cancer.Frontiers in endocrinology · 2015Review
- Article
- Nuclear receptor coactivators: master regulators of human health and disease.Annual review of medicine · 2014Review
- Dual regulation of Myc by Abl.Oncogene · 2013Article
- Transcriptional repression of AIB1 by FoxG1 leads to apoptosis in breast cancer cells.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Role of nuclear receptor coactivator 3 (Ncoa3) in pluripotency maintenance.The Journal of biological chemistry · 2012Article
- Steroid receptor coactivator-3 as a potential molecular target for cancer therapy.Expert opinion on therapeutic targets · 2012Review
- The role of AIB1 in breast cancer.Oncology letters · 2012Article
- Preclinical and clinical studies of estrogen deprivation support the PDGF/Abl pathway as a novel therapeutic target for overcoming endocrine resistance in breast cancer.Breast cancer research : BCR · 2012Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Overexpression and activation of the steroid receptor coactivator amplified in breast cancer 1 (AIB1)/steroid receptor coactivator-3 (SRC-3) have been shown to have a critical role in oncogenesis and are required for both steroid and growth factor signaling in epithelial tumors. Here, we report a new mechanism for activation of SRC coactivators. We demonstrate regulated tyrosine phosphorylation of AIB1/SRC-3 at a C-terminal tyrosine residue (Y1357) that is phosphorylated after insulin-like growth factor 1, epidermal growth factor, or estrogen treatment of breast cancer cells. Phosphorylated Y1357 is increased in HER2/neu (v-erb-b2 erythroblastic leukemia viral oncogene homolog 2) mammary tumor epithelia and is required to modulate AIB1/SRC-3 coactivation of estrogen receptor alpha (ERalpha), progesterone receptor B, NF-kappaB, and AP-1-dependent promoters. c-Abl (v-Abl Abelson murine leukemia viral oncogene homolog 1) tyrosine kinase directly phosphorylates AIB1/SRC-3 at Y1357 and modulates the association of AIB1 with c-Abl, ERalpha, the transcriptional cofactor p300, and the methyltransferase coactivator-associated arginine methyltransferase 1, CARM1. AIB1/SRC-3-dependent transcription and phenotypic changes, such as cell growth and focus formation, can be reversed by an Abl kinase inhibitor, imatinib. Thus, the phosphorylation state of Y1357 can function as a molecular on/off switch and facilitates the cross talk between hormone, growth factor, and intracellular kinase signaling pathways in cancer.
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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.