ArticleThe Journal of biological chemistry2010
BCAR3 regulates Src/p130 Cas association, Src kinase activity, and breast cancer adhesion signaling.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- Deciphering the Role of BCAR3 in Cancer Progression: Gene Regulation, Signal Transduction, and Therapeutic Implications.Cancers · 2024Review
- Localized Administration of Bcar3 siRNA via Nano-Self-Assembly to Treat Idiopathic Pulmonary Fibrosis by Disrupting Macrophage-Fibroblast Crosstalk.International journal of nanomedicine · 2024Article
- Heterocellular N-cadherin junctions enable nontransformed cells to inhibit the growth of adjacent transformed cells.Cell communication and signaling : CCS · 2022Article
- 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
- Breast cancer antiestrogen resistance 3-p130Oncogene · 2016Article
- Breast cancer anti-estrogen resistance 3 inhibits transforming growth factor β/Smad signaling and associates with favorable breast cancer disease outcomes.Breast cancer research : BCR · 2014Article
- Overcoming EMT-associated resistance to anti-cancer drugs via Src/FAK pathway inhibition.Oncotarget · 2014Article
- SRChing for the substrates of Src.Oncogene · 2014Review
- Association of the breast cancer antiestrogen resistance protein 1 (BCAR1) and BCAR3 scaffolding proteins in cell signaling and antiestrogen resistance.The Journal of biological chemistry · 2014Article
- Heparanase promotes human gastric cancer cells migration and invasion by increasing Src and p38 phosphorylation expression.International journal of clinical and experimental pathology · 2014Article
- Article
- Protein tyrosine phosphatase α phosphotyrosyl-789 binds BCAR3 to position Cas for activation at integrin-mediated focal adhesions.Molecular and cellular biology · 2012Article
- Breast cancer anti-estrogen resistance 3 (BCAR3) protein augments binding of the c-Src SH3 domain to Crk-associated substrate (p130cas).The Journal of biological chemistry · 2012Article
- NSP-CAS Protein Complexes: Emerging Signaling Modules in Cancer.Genes & cancer · 2012Article
- NSP-Cas protein structures reveal a promiscuous interaction module in cell signaling.Nature structural & molecular biology · 2011Article
- Targeting SRC in mucinous ovarian carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011Article
- The SH2 domain protein Shep1 regulates the in vivo signaling function of the scaffolding protein Cas.Cellular signalling · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The nonreceptor protein-tyrosine kinase c-Src is frequently overexpressed and/or activated in a variety of cancers, including those of the breast. Several heterologous binding partners of c-Src have been shown to regulate its catalytic activity by relieving intramolecular autoinhibitory interactions. One such protein, p130(Cas) (Cas), is expressed at high levels in both breast cancer cell lines and breast tumors, providing a potential mechanism for c-Src activation in breast cancers. The Cas-binding protein BCAR3 (breast cancer antiestrogen resistance-3) is expressed at high levels in invasive breast cancer cell lines, and this molecule has previously been shown to coordinate with Cas to increase c-Src activity in COS-1 cells. In this study, we show for the first time using gain- and loss-of-function approaches that BCAR3 regulates c-Src activity in the endogenous setting of breast cancer cells. We further show that BCAR3 regulates the interaction between Cas and c-Src, both qualitatively as well as quantitatively. Finally, we present evidence that the coordinated activity of these proteins contributes to breast cancer cell adhesion signaling and spreading. Based on these data, we propose that the c-Src/Cas/BCAR3 signaling axis is a prominent regulator of c-Src activity, which in turn controls cell behaviors that lead to aggressive and invasive breast tumor phenotypes.
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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.