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Inhibition of focal adhesion kinase by antisense oligonucleotides enhances the sensitivity of breast cancer cells to camptothecins Biocell
Satoh,Taroh H.; Surmacz,Tatiana A.; Nyormoi,Okot; Whitacre,Cecilia M..
This study shows a strong association between cell attachment to substratum and activation of b1-integrin-signaling with resistance to the camptothecin derivative topotecan (TPT) in breast cancer cells. We propose a mechanistic-driven approach to sensitize the cells to camptothecins. ZR-75-1 anchorage-dependent breast cancer cell line, its derivative 9D3S suspension cells (9D3S-S), and 9D3S cells attached to fibronectin-coated plates (9D3S-A) were treated with TPT (1 mM) or CPT-11 (40 mM) for 48 h. Programmed cell death (PCD), as shown by poly(ADP-ribose) polymerase (PARP), pro-caspase-3 and pro-caspase-9 cleavage, was observed in 9D3S-S cells but not in ZR-75-1 or 9D3S-A cells. Because p125 focal adhesion kinase (FAK) is a transducer in the b1-integrin...
Tipo: Info:eu-repo/semantics/article Palavras-chave: Focal adhesion kinase; Drug resistance; Camptothecins; Breast cancer.
Ano: 2003 URL: http://www.scielo.org.ar/scielo.php?script=sci_arttext&pid=S0327-95452003000100006
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Focal adhesion kinase signaling in cardiac hypertrophy and failure BJMBR
Franchini,K.G.; Clemente,C.F.M.Z.; Marin,T.M..
Focal adhesion kinase (FAK) is a broadly expressed tyrosine kinase implicated in cellular functions such as migration, growth and survival. Emerging data support a role for FAK in cardiac development, reactive hypertrophy and failure. Data reviewed here indicate that FAK plays a critical role at the cellular level in the responses of cardiomyocytes and cardiac fibroblasts to biomechanical stress and to hypertrophic agonists such as angiotensin II and endothelin. The signaling mechanisms regulated by FAK are discussed to provide insight into its role in the pathophysiology of cardiac hypertrophy and failure.
Tipo: Info:eu-repo/semantics/article Palavras-chave: Focal adhesion kinase; Mechanical signaling; Cardiovascular system; Signal transduction.
Ano: 2009 URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2009000100008
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