BCAR1/p130Cas expression in untreated and acquired tamoxifen-resistant human breast carcinomas

Flier, S. van der; Chan, Christina M.W.; Brinkman, Arend; Smid, Marcel; Johnston, Stephen; Dorssers, Lambert C. J.; Dowsett, Mitchell

doi:10.1002/1097-0215(20000920)89:5<465::aid-ijc11>3.0.co;2-o

Cited by 42 publications

(27 citation statements)

References 26 publications

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“…Crk is an adaptor protein that regulates cells spreading and migration by coupling critical signaling proteins such as EGFR, PDGFR, and C-Abl to the cytoskeleton and focal adhesions including the scaffolding protein p130Cas (47). p130Cas and its family members are necessary for cell migration and cancer cell invasion and have been associated with cancer progression in patients (48)(49)(50)(51). Interestingly, p130Cas coprecipitates with PEAK1 and PEAK1 modulates p130Cas-Y249 phosphorylation (Fig.…”

Section: Discussionmentioning

confidence: 99%

Pseudopodium-enriched atypical kinase 1 regulates the cytoskeleton and cancer progression

Wang¹,

Kelber²,

Cao³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

109

190

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Regulation of the actin-myosin cytoskeleton plays a central role in cell migration and cancer progression. Here, we report the discovery of a cytoskeleton-associated kinase, pseudopodium-enriched atypical kinase 1 (PEAK1). PEAK1 is a 190-kDa nonreceptor tyrosine kinase that localizes to actin filaments and focal adhesions. PEAK1 undergoes Src-induced tyrosine phosphorylation, regulates the p130Cas-Crk-paxillin and Erk signaling pathways, and operates downstream of integrin and epidermal growth factor receptors (EGFR) to control cell spreading, migration, and proliferation. Perturbation of PEAK1 levels in cancer cells alters anchorage-independent growth and tumor progression in mice. Notably, primary and metastatic samples from colon cancer patients display amplified PEAK1 levels in 81% of the cases. Our findings indicate that PEAK1 is an important cytoskeletal regulatory kinase and possible target for anticancer therapy.

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Section: Discussionmentioning

confidence: 99%

Pseudopodium-enriched atypical kinase 1 regulates the cytoskeleton and cancer progression

Wang¹,

Kelber²,

Cao³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

109

190

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“…Indeed p130CAS silencing in ERBB2 transformed breast cancer cells is sufficient to inhibit tumour growth in vivo, and correlates with downregulation of proliferative and survival pathways, such as SRC and AKT activation, focal adhesion kinase (FAK) phosphorylation and CYCLIN D1 expression 11 . In oestrogen receptor (ER)-positive human breast tumours, overexpression of p130CAS correlates with intrinsic resistance to tamoxifen treatment in a large subset of human breast cancer samples [15][16][17] .…”

Section: Integrin Adaptors In Cancermentioning

confidence: 99%

Integrin signalling adaptors: not only figurants in the cancer story

et al. 2010

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Current evidence highlights the ability of adaptor (or scaffold) proteins to create signalling platforms that drive cellular transformation upon integrin-dependent adhesion and growth factor receptor activation. The understanding of the biological effects regulated by these adaptors in tumours might be crucial for the identification of novel targets and the development of innovative therapeutic strategies for human cancer. In this review we will discuss the relevance of adaptor proteins in signalling originating from integrin-mediated cell-extracellular matrix (ECM) adhesion and growth factor stimulation within the context of cell transformation and tumour progression.Herein, we will specifically underline the contribution of p130CAS, NEDD9, CRK, and the IPP complex (ILK, PINCH and PARVIN) to cancer, along with the more recently identified p140CAP.

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“…Recently, BCAR1 has also been implicated in resistance to the chemotherapeutic drug adriamycin [13]. Furthermore, by analysis of patient specimens we have shown that patients with primary breast tumors containing high BCAR1 protein levels have a poor prognosis and a poor type of response to tamoxifen treatment [14][15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

The substrate domain of BCAR1 is essential for anti-estrogen-resistant proliferation of human breast cancer cells

Brinkman

Jong

Tuinman

et al. 2009

Breast Cancer Res Treat

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BCAR1/p130Cas expression in untreated and acquired tamoxifen-resistant human breast carcinomas

Cited by 42 publications

References 26 publications

Pseudopodium-enriched atypical kinase 1 regulates the cytoskeleton and cancer progression

Pseudopodium-enriched atypical kinase 1 regulates the cytoskeleton and cancer progression

Integrin signalling adaptors: not only figurants in the cancer story

The substrate domain of BCAR1 is essential for anti-estrogen-resistant proliferation of human breast cancer cells

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