ArticleEMBO reports2020
Loss of ANCO1 repression at AIB1/YAP targets drives breast cancer progression.
Article in EMBO reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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
20 citing papers in PubMed, 24 citations in OpenAlex.
- Yorkie/YAP Interactors: Fine-Tuning the Hippo Pathway Output.Cold Spring Harbor perspectives in biology · 2026Article
- An AIB1 isoform rewires glucocorticoid receptor signaling to promote TNBC progression.iScience · 2026Article
- Article
- Targeting TEAD in cancer.Frontiers in oncology · 2025Review
- The oncogenic axis YAP/MYC/EZH2 impairs PTEN tumor suppression activity enhancing lung tumorigenicity.Cell death discovery · 2024Article
- 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 biology of YAP in programmed cell death.Biomarker research · 2022Review
- Spatial collagen stiffening promotes collective breast cancer cell invasion by reinforcing extracellular matrix alignment.Oncogene · 2022Article
- Endocrine resistance in breast cancer: from molecular mechanisms to therapeutic strategies.Journal of molecular medicine (Berlin, Germany) · 2021Review
- An AIB1 Isoform Alters Enhancer Access and Enables Progression of Early-Stage Triple-Negative Breast Cancer.Cancer research · 2021Article
- Metastasis-suppressor NME1 controls the invasive switch of breast cancer by regulating MT1-MMP surface clearance.Oncogene · 2021Article
- SRC-3, a Steroid Receptor Coactivator: Implication in Cancer.International journal of molecular sciences · 2021Review
- Phosphorylation of steroid receptor coactivator-3 (SRC-3) at serine 857 is regulated by the p38Scientific reports · 2020Article
- 17‑AAG synergizes with Belinostat to exhibit a negative effect on the proliferation and invasion of MDA‑MB‑231 breast cancer cells.Oncology reports · 2020Article
- One repressor to rule them all: ANCO1 links YAP and AIB1.EMBO reports · 2020Article
- Article
- The relationship between TRAF6 and tumors.Cancer cell international · 2020Review
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Transcription factors critical for the transition of normal breast epithelium to ductal carcinoma in situ (DCIS) and invasive breast cancer are not clearly defined. Here, we report that the expression of a subset of YAP-activated and YAP-repressed genes in normal mammary and early-stage breast cancer cells is dependent on the nuclear co-activator AIB1. Gene expression, sequential ChIP, and ChIP-seq analyses show that AIB1 and YAP converge upon TEAD for transcriptional activation and repression. We find that AIB1-YAP repression of genes at the 1q21.3 locus is mediated by AIB1-dependent recruitment of ANCO1, a tumor suppressor whose expression is progressively lost during breast cancer progression. Reducing ANCO1 reverts AIB1-YAP-dependent repression, increases cell size, and enhances YAP-driven aberrant 3D growth. Loss of endogenous ANCO1 occurs during DCIS xenograft progression, a pattern associated with poor prognosis in human breast cancer. We conclude that increased expression of AIB1-YAP co-activated targets coupled with a loss of normal ANCO1 repression is critical to patterns of gene expression that mediate malignant progression of early-stage 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.