ArticleCancer research2010
Estrogen-dependent and estrogen-independent mechanisms contribute to AIB1-mediated tumor formation.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 53 citations in OpenAlex.
- Steroid receptor coactivators: from basic research to translational opportunities.Endocrine reviews · 2026Review
- Steroid receptor coactivators in immunity - From function to emerging translational opportunities.The Journal of biological chemistry · 2026Review
- Steroid receptor coactivator 1 promotes human hepatocellular carcinoma invasiveness through enhancing MMP-9.Journal of cellular and molecular medicine · 2024Article
- Critical Roles of SRC-3 in the Development and Progression of Breast Cancer, Rendering It a Prospective Clinical Target.Cancers · 2023Review
- High FOXA1 levels induce ER transcriptional reprogramming, a pro-metastatic secretome, and metastasis in endocrine-resistant breast cancer.Cell reports · 2023Article
- The chemokine monocyte chemoattractant protein-1/CCL2 is a promoter of breast cancer metastasis.Cellular & molecular immunology · 2023Review
- Significant Association of Estrogen Receptor-β Isoforms and Coactivators in Breast Cancer Subtypes.Current issues in molecular biology · 2023Article
- Functional and Phenotypic Characterisations of Common Syngeneic Tumour Cell Lines as Estrogen Receptor-Positive Breast Cancer Models.International journal of molecular sciences · 2023Article
- AIB1/SRC-3/NCOA3 function in estrogen receptor alpha positive breast cancer.Frontiers in endocrinology · 2023Review
- Estrogen-induced immune changes within the normal mammary gland.Scientific reports · 2022Article
- SRC-3, a Steroid Receptor Coactivator: Implication in Cancer.International journal of molecular sciences · 2021Review
- Article
- Cytoplasmic ERα and NFκB Promote Cell Survival in Mouse Mammary Cancer Cell Lines.Hormones & cancer · 2020Article
- Exogenous ERα Expression in the Mammary Epithelium Decreases Over Time and Does Not Contribute to p53-Deficient Mammary Tumor Formation in Mice.Journal of mammary gland biology and neoplasia · 2019Article
- The Emerging Roles of Steroid Hormone Receptors in Ductal Carcinoma in Situ (DCIS) of the Breast.Journal of mammary gland biology and neoplasia · 2018Review
- Plac1 Is a Key Regulator of the Inflammatory Response and Immune Tolerance In Mammary Tumorigenesis.Scientific reports · 2018Article
- Cancer Stem Cell Phenotypes in ERMolecular cancer research : MCR · 2018Article
- Embryonic transcription factor SOX9 drives breast cancer endocrine resistance.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Role of steroid receptor and coregulator mutations in hormone-dependent cancers.The Journal of clinical investigation · 2017Review
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
We have previously reported the oncogenic properties of the gene amplified in breast cancer 1 (AIB1), a member of the p160 family of hormone receptor coactivators. In a transgenic mouse model, AIB1 overexpression resulted in a high incidence of tumors in various tissues, including mammary gland, uterus, lung, and pituitary. To determine whether the AIB1 oncogenicity in this model depended on its function as an estrogen receptor (ER) coactivator, we abolished ER signaling through two independent approaches, by performing ovariectomy on AIB1 transgenic (AIB1-tg) mice to prevent gonadal estrogen production and by crossing AIB1-tg mice with ERalpha-null mutant mice. Ovariectomized (ovx) mice, but not AIB1 x ERalpha-/- mice, still developed mammary gland hyperplasia and ductal carcinoma in situ. Both approaches, however, completely prevented the development of invasive mammary tumors, indicating that invasive mammary tumor formation is strictly estrogen dependent. Once developed, AIB1-induced mammary tumors can subsequently lose their dependence on estrogen: Injection of ERalpha(+) tumor cell lines derived from such tumors into ovx or untreated wild-type mice resulted in a similar rate of tumor growth in both groups. Surprisingly, however, ovx mice had an approximately 4-fold higher rate of metastasis formation, suggesting that estrogen provided some protection from metastasis formation. Lastly, our experiments identified oncogenic functions of AIB1 that are independent of its ER coactivation, as both approaches, ovariectomy and ER-/- crosses, still resulted in a high incidence of tumors in the lung and pituitary. We therefore conclude that AIB1 can exert its oncogenicity through tissue-specific estrogen-dependent and estrogen-independent functions.
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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.