ArticlePLoS biology2011
Interplay between BRCA1 and RHAMM regulates epithelial apicobasal polarization and may influence risk of breast cancer.
Article in PLoS biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 193 citations in OpenAlex.
- RHAMM drives formation of polyploid cancer cells and confers resistance to ER-targeted therapy in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Co-Pathogenic Role of BRCA1 and OBSCN Deletions in Chinese Familial Breast Cancer: A Case Report.The American journal of case reports · 2026Article
- HMMR in human cancers: regulatory mechanism and biological function.Journal of translational medicine · 2025Review
- Targeting RHAMM in Cancer: Crosstalk with Non-Coding RNAs and Emerging Therapeutic Strategies Including Peptides, Oligomers, Antibodies, and Vaccines.International journal of molecular sciences · 2025Review
- Mutational landscape of pure ductal carcinoma in situ and associations with disease prognosis and response to radiotherapy.Breast cancer research : BCR · 2025Article
- Dual targeting of Aurora Kinase A and poly (ADP-ribose) polymerase as a therapeutic option for patients with ovarian cancer: preclinical evaluations.Journal of cancer research and clinical oncology · 2025Article
- Harnessing transcriptional regulation of alternative end-joining to predict cancer treatment.NAR cancer · 2025Article
- CoGTEx: Unscaled system-level coexpression estimation from GTEx data forecast novel functional gene partners.PloS one · 2024Article
- Hyaluronan Receptors as Mediators and Modulators of the Tumor Microenvironment.Advanced healthcare materials · 2023Review
- Pathogenic BRCA1 variants disrupt PLK1-regulation of mitotic spindle orientation.Nature communications · 2022Article
- Modification of BRCA1-associated breast cancer risk by HMMR overexpression.Nature communications · 2022Article
- Review
- CDK5RAP3, a New BRCA2 Partner That Regulates DNA Repair, Is Associated with Breast Cancer Survival.Cancers · 2022Article
- The role of RHAMM in cancer: Exposing novel therapeutic vulnerabilities.Frontiers in oncology · 2022Review
- HMMR potential as a diagnostic and prognostic biomarker of cancer-speculation based on a pan-cancer analysis.Frontiers in surgery · 2022Article
- Human iPSC-derived fallopian tube organoids with BRCA1 mutation recapitulate early-stage carcinogenesis.Cell reports · 2021Article
- Review
- Directed movement toward, translocation along, penetration into and exit from vascular networks by breast cancer cells in 3D.Cell adhesion & migration · 2021Article
- AR-mTOR-SRF Axis Regulates HMMR Expression in Human Prostate Cancer Cells.Biomolecules & therapeutics · 2021Article
- Extracellular matrix and its therapeutic potential for cancer treatment.Signal transduction and targeted therapy · 2021Review
3 more citing papers are in PubMed but not listed here.
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Authors and funding
150 authors at 20 institutions in 18 countries.
Funding
Abstract
Differentiated mammary epithelium shows apicobasal polarity, and loss of tissue organization is an early hallmark of breast carcinogenesis. In BRCA1 mutation carriers, accumulation of stem and progenitor cells in normal breast tissue and increased risk of developing tumors of basal-like type suggest that BRCA1 regulates stem/progenitor cell proliferation and differentiation. However, the function of BRCA1 in this process and its link to carcinogenesis remain unknown. Here we depict a molecular mechanism involving BRCA1 and RHAMM that regulates apicobasal polarity and, when perturbed, may increase risk of breast cancer. Starting from complementary genetic analyses across families and populations, we identified common genetic variation at the low-penetrance susceptibility HMMR locus (encoding for RHAMM) that modifies breast cancer risk among BRCA1, but probably not BRCA2, mutation carriers: n = 7,584, weighted hazard ratio ((w)HR) = 1.09 (95% CI 1.02-1.16), p(trend) = 0.017; and n = 3,965, (w)HR = 1.04 (95% CI 0.94-1.16), p(trend) = 0.43; respectively. Subsequently, studies of MCF10A apicobasal polarization revealed a central role for BRCA1 and RHAMM, together with AURKA and TPX2, in essential reorganization of microtubules. Mechanistically, reorganization is facilitated by BRCA1 and impaired by AURKA, which is regulated by negative feedback involving RHAMM and TPX2. Taken together, our data provide fundamental insight into apicobasal polarization through BRCA1 function, which may explain the expanded cell subsets and characteristic tumor type accompanying BRCA1 mutation, while also linking this process to sporadic breast cancer through perturbation of HMMR/RHAMM.
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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.