ArticleJournal of cellular physiology2011
Ubc9 mediates nuclear localization and growth suppression of BRCA1 and BRCA1a proteins.
Article in Journal of cellular physiology, 2011. 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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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- DNA end-resection is stimulated by an interaction between BRCA1 exon 11 and TOPBP1.EMBO reports · 2026Article
- Identification of UBE2I as a Novel Biomarker in ccRCC Based on a Large-Scale CRISPR-Cas9 Screening Database and Immunohistochemistry.Frontiers in molecular biosciences · 2022Article
- Constitutively active androgen receptor supports the metastatic phenotype of endocrine-resistant hormone receptor-positive breast cancer.Cell communication and signaling : CCS · 2020Article
- TheGenes · 2019Article
- BRCA1-No Matter How You Splice It.Cancer research · 2019Review
- DNA damage and tissue repair: What we can learn from planaria.Seminars in cell & developmental biology · 2019Review
- A Provocative Molecular Link between Mammographic Density and BRCA1-loss associated TNBC.International journal of human genetics and genetic disorders · 2019Article
- Assessing predictions of fitness effects of missense mutations in SUMO-conjugating enzyme UBE2I.Human mutation · 2017Article
- A novel Ubc9 -dependent pathway regulates SIRT1- ER-α Axis and BRCA1-associated TNBC lung metastasis.Integrative molecular medicine · 2017Article
- BRCA1 Mutation Leads to Deregulated Ubc9 Levels which Triggers Proliferation and Migration of Patient-Derived High Grade Serous Ovarian Cancer and Triple Negative Breast Cancer Cells.International journal of chronic diseases & therapy · 2016Article
- miR-200c-SUMOylated KLF4 feedback loop acts as a switch in transcriptional programs that control VSMC proliferation.Journal of molecular and cellular cardiology · 2015Article
- BRCA1 EXON 11, a CERES (composite regulatory element of splicing) element involved in splice regulation.International journal of molecular sciences · 2014Article
- Polymorphism of UBC9 gene encoding the SUMO-E2-conjugating enzyme and breast cancer risk.Pathology oncology research : POR · 2014Article
- Identification of a non-canonical nuclear localization signal (NLS) in BRCA1 that could mediate nuclear localization of splice variants lacking the classical NLS.Cellular & molecular biology letters · 2013Article
- Ubiquitin- and ubiquitin-like proteins-conjugating enzymes (E2s) in breast cancer.Molecular biology reports · 2013Article
- Triple Negative Breast Cancer - An Overview.Hereditary genetics : current research · 2013Article
- The BRCA1 Breast Cancer Suppressor: Regulation of Transport, Dynamics, and Function at Multiple Subcellular Locations.Scientifica · 2012Review
- Article
- BRCA1 proteins regulate growth of ovarian cancer cells by tethering Ubc9.American journal of cancer research · 2012Article
- A Novel Pathway that Links Caveolin-1 Down-Regulation to BRCA1 Dysfunction in Serous Epithelial Ovarian Cancer Cells.Enliven. Challenges in cancer detection and therapyArticle
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
BRCA1 gene mutations are responsible for hereditary breast and ovarian cancers. In sporadic breast tumors, BRCA1 dysfunction or aberrant subcellular localization is thought to be common. BRCA1 is a nuclear-cytoplasm shuttling protein and the reason for cytoplasmic localization of BRCA1 in young breast cancer patients is not yet known. We have previously reported BRCA1 proteins unlike K109R and cancer-predisposing mutant C61G to bind Ubc9 and modulate ER-α turnover. In the present study, we have examined the consequences of altered Ubc9 binding and knockdown on the subcellular localization and growth inhibitory function of BRCA1 proteins. Our results using live imaging of YFP, GFP, RFP-tagged BRCA1, BRCA1a and BRCA1b proteins show enhanced cytoplasmic localization of K109 R and C61G mutant BRCA1 proteins in normal and cancer cells. Furthermore, down-regulation of Ubc9 in MCF-7 cells using Ubc9 siRNA resulted in enhanced cytoplasmic localization of BRCA1 protein and exclusive cytoplasmic retention of BRCA1a and BRCA1b proteins. These mutant BRCA1 proteins were transforming and impaired in their capacity to inhibit growth of MCF-7 and CAL51 breast cancer cells. Interestingly, cytoplasmic BRCA1a mutants showed more clonogenicity in soft agar and higher levels of expression of Ubc9 than parental MCF7 cells. This is the first report demonstrating the physiological link between cytoplasmic mislocalization of mutant BRCA1 proteins, loss of ER-α repression, loss of ubiquitin ligase activity and loss of growth suppression of BRCA1 proteins. Thus, binding of BRCA1 proteins to nuclear chaperone Ubc9 provides a novel mechanism for nuclear import and control of tumor growth.
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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.