ArticlePloS one2013
Breast cancer antiestrogen resistance 3 (BCAR3) promotes cell motility by regulating actin cytoskeletal and adhesion remodeling in invasive breast cancer cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- Deciphering the Role of BCAR3 in Cancer Progression: Gene Regulation, Signal Transduction, and Therapeutic Implications.Cancers · 2024Review
- Proteogenomic analysis reveals cytoplasmic sequestration of RUNX1 by the acute myeloid leukemia-initiating CBFB::MYH11 oncofusion protein.The Journal of clinical investigation · 2023Article
- Fyn-Mediated Paxillin Tyrosine 31 Phosphorylation Regulates Migration and Invasion of Breast Cancer Cells.International journal of molecular sciences · 2023Article
- Proteolytic regulation of a galectin-3/Lrp1 axis controls osteoclast-mediated bone resorption.The Journal of cell biology · 2023Article
- Evidence for virus-mediated oncogenesis in bladder cancers arising in solid organ transplant recipients.eLife · 2023Article
- Article
- Comprehensive immunohistochemical analysis of RET, BCAR1, and BCAR3 expression in patients with Luminal A and B breast cancer subtypes.Breast cancer research and treatment · 2022Article
- Catulin Based Reporter System to Track and Characterize the Population of Invasive Cancer Cells in the Head and Neck Squamous Cell Carcinoma.International journal of molecular sciences · 2021Article
- BCAR3 promotes head and neck cancer growth and is associated with poor prognosis.Cell death discovery · 2021Article
- Article
- Breast Cancer Antiestrogen Resistance 3 (BCAR3) promotes tumor growth and progression in triple-negative breast cancer.American journal of cancer research · 2021Article
- Diversification of piRNAs expressed in PGCs and somatic cells during embryonic gonadal development.RNA biology · 2020Article
- Melittin fromAntibiotics (Basel, Switzerland) · 2020Article
- A proximity-labeling proteomic approach to investigate invadopodia molecular landscape in breast cancer cells.Scientific reports · 2020Article
- Integrative omics analysis identifies macrophage migration inhibitory factor signaling pathways underlying human hepatic fibrogenesis and fibrosis.Journal of bio-X research · 2019Article
- Prediction and prognostic significance of BCAR3 expression in patients with multiple myeloma.Journal of translational medicine · 2018Article
- Breast cancer antiestrogen resistance 3-p130Oncogene · 2016Article
- Long noncoding RNA are aberrantly expressed in human papillary thyroid carcinoma.Oncology letters · 2016Article
- Expression pattern of bcar3, a downstream target of Gata2, and its binding partner, bcar1, during Xenopus development.Gene expression patterns : GEP · 2016Article
- Epigenetic inactivation of SOX1 promotes cell migration in lung cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Metastatic breast cancer is incurable. In order to improve patient survival, it is critical to develop a better understanding of the molecular mechanisms that regulate metastasis and the underlying process of cell motility. Here, we focus on the role of the adaptor molecule Breast Cancer Antiestrogen Resistance 3 (BCAR3) in cellular processes that contribute to cell motility, including protrusion, adhesion remodeling, and contractility. Previous work from our group showed that elevated BCAR3 protein levels enhance cell migration, while depletion of BCAR3 reduces the migratory and invasive capacities of breast cancer cells. In the current study, we show that BCAR3 is necessary for membrane protrusiveness, Rac1 activity, and adhesion disassembly in invasive breast cancer cells. We further demonstrate that, in the absence of BCAR3, RhoA-dependent signaling pathways appear to predominate, as evidenced by an increase in RhoA activity, ROCK-mediated phosphorylation of myosin light chain II, and large ROCK/mDia1-dependent focal adhesions. Taken together, these data establish that BCAR3 functions as a positive regulator of cytoskeletal remodeling and adhesion turnover in invasive breast cancer cells through its ability to influence the balance between Rac1 and RhoA signaling. Considering that BCAR3 protein levels are elevated in advanced breast cancer cell lines and enhance breast cancer cell motility, we propose that BCAR3 functions in the transition to advanced disease by triggering intracellular signaling events that are essential to the metastatic process.
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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.