ArticleBreast cancer research : BCR2018
Estrogen promotes estrogen receptor negative BRCA1-deficient tumor initiation and progression.
Article in Breast cancer research : BCR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 49 citations in OpenAlex.
- The PER2:BRCA1:POU2F1(OCT-1) ternary complex represents a multi-component scaffold model for circadian gene regulation.Neurobiology of sleep and circadian rhythms · 2026Article
- Natural menopause, menarche and breast cancer risk in BRCA1 and BRCA2 pathogenic variant carriers: a Mendelian randomization analysis.British journal of cancer · 2026Article
- Endogenous and environmental factors that induce DNA replication defects and genomic instability in ER-negative heterozygous BRCA1 cells.Scientific reports · 2026Article
- Medroxyprogesterone Acetate Inhibits Tumorigenesis in Mouse Models of Oviductal High-Grade Serous Carcinoma.Cancers · 2025Article
- Article
- The Tumour Microenvironment and Epigenetic Regulation inCancers · 2024Review
- GATA3 functions downstream of BRCA1 to promote DNA damage repair and suppress dedifferentiation in breast cancer.BMC biology · 2024Article
- Estrogen Receptor Signaling in Breast Cancer.Cancers · 2023Review
- Impaired histone inheritance promotes tumor progression.Nature communications · 2023Article
- Proteomic Markers for Mechanobiological Properties of Metastatic Cancer Cells.International journal of molecular sciences · 2023Review
- Survival outcomes of metastatic breast cancer patients by germline BRCA1/2 status in a large multicenter real-world database.International journal of cancer · 2023Article
- Loss of function of BRCA1 promotes EMT in mammary tumors through activation of TGFβR2 signaling pathway.Cell death & disease · 2022Article
- Review
- Loss of function of GATA3 induces basal-like mammary tumors.Theranostics · 2022Article
- Efficacy, Safety, and Prognosis of Sequential Therapy with Tamoxifen and Letrozole versus Letrozole Monotherapy for Breast Carcinoma.Computational and mathematical methods in medicine · 2022Article
- Bilateral Salpingo-oophorectomy and Breast Cancer Risk forCancer prevention research (Philadelphia, Pa.) · 2021Review
- Clinical behavior and outcomes of breast cancer in young women with germline BRCA pathogenic variants.NPJ breast cancer · 2021Article
- The Role ofCancers · 2021Review
- PDGFRβ is an essential therapeutic target for BRCA1-deficient mammary tumors.Breast cancer research : BCR · 2021Article
- GATA3 functions downstream of BRCA1 to suppress EMT in breast cancer.Theranostics · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEstrogen promotes breast cancer development and progression mainly through estrogen receptor (ER). However, blockage of estrogen production or action prevents development of and suppresses progression of ER-negative breast cancers. How estrogen promotes ER-negative breast cancer development and progression is poorly understood. We previously discovered that deletion of cell cycle inhibitors p16
methodsA genetic model system with three mouse strains, one that develops ER-positive mammary tumors (p18 single deletion) and the others that develop ER-negative tumors (p16;Brca1 and p18;Brca1 compound deletion), human BRCA1 mutant breast cancer patient-derived xenografts, and human BRCA1-deficient and BRCA1-proficient breast cancer cells were used to determine the role of estrogen in activating epithelial-mesenchymal transition (EMT), stimulating cell proliferation, and promoting ER-negative mammary tumor initiation and metastasis.
resultsEstrogen stimulated the proliferation and tumor-initiating potential of both ER-positive Brca1-proficient and ER-negative Brca1-deficient tumor cells. Estrogen activated EMT in a subset of Brca1-deficient mammary tumor cells that maintained epithelial features, and enhanced the number of cancer stem cells, promoting tumor progression and metastasis. Estrogen activated EMT independent of ER in Brca1-deficient, but not Brca1-proficient, tumor cells. Estrogen activated the AKT pathway in BRCA1-deficient tumor cells independent of ER, and pharmaceutical inhibition of AKT activity suppressed EMT and cell proliferation preventing BRCA1 deficient tumor progression.
conclusionsThis study reveals for the first time that estrogen promotes BRCA1-deficient tumor initiation and progression by stimulation of cell proliferation and activation of EMT, which are dependent on AKT activation and independent of ER.
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