ArticleMolecular endocrinology (Baltimore, Md.)2014
Regulation of HER2 oncogene transcription by a multifunctional coactivator/corepressor complex.
Article in Molecular endocrinology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Dysfunction of a SET3-like complex underlies a family of related neurological disorders.Nature communications · 2026Article
- An AIB1 isoform rewires glucocorticoid receptor signaling to promote TNBC progression.iScience · 2026Article
- Review
- KBG syndrome-associated protein ANKRD11 regulates SETD5 expression to modulate rRNA levels and translation.iScience · 2025Article
- The role of ankyrin repeat-containing proteins in epigenetic and transcriptional regulation.Cell death discovery · 2025Review
- Insights into the ANKRD11 variants and short-stature phenotype through literature review and ClinVar database search.Orphanet journal of rare diseases · 2024Review
- Subpopulations of AIB1 isoform-expressing breast cancer cells enable invasion and metastasis.Oncotarget · 2023Article
- Loss of ANCO1 Expression Regulates Chromatin Accessibility and Drives Progression of Early-Stage Triple-Negative Breast Cancer.International journal of molecular sciences · 2023Article
- AIB1/SRC-3/NCOA3 function in estrogen receptor alpha positive breast cancer.Frontiers in endocrinology · 2023Review
- The potential of mRNA expression evaluation in predicting HER2 positivity in gastroesophageal cancer.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2022Article
- An AIB1 Isoform Alters Enhancer Access and Enables Progression of Early-Stage Triple-Negative Breast Cancer.Cancer research · 2021Article
- Article
- Article
- Modeling Neoadjuvant chemotherapy resistance in vitro increased NRP-1 and HER2 expression and converted MCF7 breast cancer subtype.British journal of pharmacology · 2020Article
- One repressor to rule them all: ANCO1 links YAP and AIB1.EMBO reports · 2020Article
- Article
- Germline and SomaticCancer prevention research (Philadelphia, Pa.) · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Transcription of the HER2 oncogene can be repressed by estrogen (E2). We now show that, a splice isoform of the nuclear receptor coactivator AIB1, AIB1-Δ4, is able to reverse E2 repression of HER2 gene expression in breast cancer cells. The first 224 amino acids of AIB1 that are absent in AIB1-Δ4, bind a co-repressor, ANCO1. Using chromatin immunoprecipitation assay approaches in MCF7 and BT474 cell lines, we demonstrate that AIB1 and AIB1-Δ4 can bind to the E2 regulatory site in the first intron of the HER2 gene, after E2 treatment, but only full-length AIB1 recruits ANCO1. Consistent with E2-induced chromatin repression, the AIB1-ANCO1 complex recruits HDAC3 and HDAC4 to the intronic estrogen response element and the proximal promoter acquires the repressive chromatin mark H3K9me3 and loses H3K4me1. In contrast, AIB1-Δ4 does not recruit ANCO 1, HDAC3, or HDAC4 and the proximal promoter retains activation marks of H3K4me1. In cell lines with low levels of ANCO1 (T47D), E2 does not repress HER2 gene transcription but the repressive response can be restored by overexpression of ANCO1. ANCO1 can also repress other E2-responsive genes, indicating that AIB1, AIB1-Δ4 and ANCO1 are important determinants of endocrine and growth factor responsiveness in breast cancer.
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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.