ArticleJournal of cellular biochemistry2009
Expression of a phosphorylated p130(Cas) substrate domain attenuates the phosphatidylinositol 3-kinase/Akt survival pathway in tamoxifen resistant breast cancer cells.
Article in Journal of cellular biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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
17 citing papers in PubMed, 19 citations in OpenAlex.
- Structural and functional insights into the interaction between the Cas family scaffolding protein p130Cas and the focal adhesion-associated protein paxillin.The Journal of biological chemistry · 2017Article
- A truncated phosphorylated p130Cas substrate domain is sufficient to drive breast cancer growth and metastasis formation in vivo.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Identification of Novel Crk-associated Substrate (p130Cas) Variants with Functionally Distinct Focal Adhesion Kinase Binding Activities.The Journal of biological chemistry · 2015Article
- 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
- Cas proteins: dodgy scaffolding in breast cancer.Breast cancer research : BCR · 2014Review
- Expression of a phosphorylated substrate domain of p130Cas promotes PyMT-induced c-Src-dependent murine breast cancer progression.Carcinogenesis · 2013Article
- p130Cas acts as survival factor during PMA-induced apoptosis in HL-60 promyelocytic leukemia cells.The international journal of biochemistry & cell biology · 2013Article
- Article
- A new synthetic HDAC inhibitor, MHY218, induces apoptosis or autophagy-related cell death in tamoxifen-resistant MCF-7 breast cancer cells.Investigational new drugs · 2012Article
- NSP-CAS Protein Complexes: Emerging Signaling Modules in Cancer.Genes & cancer · 2012Article
- Roles for crk in cancer metastasis and invasion.Genes & cancer · 2012Article
- Regulation of p130(Cas)/BCAR1 expression in tamoxifen-sensitive and tamoxifen-resistant breast cancer cells by EGR1 and NAB2.Neoplasia (New York, N.Y.) · 2012Article
- Lysyl oxidase propeptide sensitizes pancreatic and breast cancer cells to doxorubicin-induced apoptosis.Journal of cellular biochemistry · 2010Article
- Dynamics and mechanism of p130Cas localization to focal adhesions.The Journal of biological chemistry · 2010Article
- CAS proteins in normal and pathological cell growth control.Cellular and molecular life sciences : CMLS · 2010Review
- Biological determinants of endocrine resistance in breast cancer.Nature reviews. Cancer · 2009Review
- p130Cas substrate domain signaling promotes migration, invasion, and survival of estrogen receptor-negative breast cancer cells.Breast cancer (Dove Medical Press) · 2009Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Elevated expression of p130(Cas)/BCAR1 (breast cancer anti estrogen resistance 1) in human breast tumors is a marker of poor prognosis and poor overall survival. Specifically, p130(Cas) signaling has been associated with antiestrogen resistance, for which the mechanism is currently unknown. TAM-R cells, which were established by long-term exposure of estrogen (E(2))-dependent MCF-7 cells to tamoxifen, displayed elevated levels of total and activated p130(Cas). Here we have investigated the effects of p130(Cas) inhibition on growth factor signaling in tamoxifen resistance. To inhibit p130(Cas), a phosphorylated substrate domain of p130(Cas), that acts as a dominant-negative (DN) p130(Cas) molecule by blocking signal transduction downstream of the p130(Cas) substrate domain, as well as knockdown by siRNA was employed. Interference with p130(Cas) signaling/expression induced morphological changes, which were consistent with a more epithelial-like phenotype. The phenotypic reversion was accompanied by reduced migration, attenuation of the ERK and phosphatidylinositol 3-kinase/Akt pathways, and induction of apoptosis. Apoptosis was accompanied by downregulation of the expression of the anti-apoptotic protein Bcl-2. Importantly, these changes re-sensitized TAM-R cells to tamoxifen treatment by inducing cell death. Therefore, our findings suggest that targeting the product of the BCAR1 gene by a peptide which mimics the phosphorylated substrate domain may provide a new molecular avenue for treatment of antiestrogen resistant breast cancers.
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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.