Inhibition of serum-stimulated mitogen activated protein kinase by 1α,25(OH)2-vitamin D3 in MCF-7 breast cancer cells

1α,25-Dihydroxyvitamin D3 [1α,25(OH) 2D3], the hormonally active form of vitamin D3, has been shown to be a potent negative growth regulator of breast cancer cells both in vitro and in vivo. 1α,25(OH)2D3 acts through two different mechanisms. In addition to regulating gene transcription via its spec...

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Autor principal: Capiati, D.A
Otros Autores: Rossi, A.M, Picotto, G., Benassati, S., Boland, R.L
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 2004
Acceso en línea:Registro en Scopus
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Registro en la Biblioteca Digital
Aporte de:Registro referencial: Solicitar el recurso aquí
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024 7 |2 scopus  |a 2-s2.0-16544373001 
024 7 |2 cas  |a calcitriol, 32222-06-3, 32511-63-0, 66772-14-3; mitogen activated protein kinase 1, 137632-08-7; mitogen activated protein kinase 3, 137632-07-6; mitogen activated protein kinase, 142243-02-5; orthovanadic acid, 14333-18-7; protein tyrosine kinase, 80449-02-1; phosphotyrosine, 21820-51-9; protein tyrosine phosphatase, 79747-53-8, 97162-86-2; 4-amino-5-(4-methylphenyl)-7-(tert-butyl)pyrazolo(3,4-d)pyrimidine; Calcitriol, 32222-06-3; Enzyme Inhibitors; Mitogen-Activated Protein Kinases, EC 2.7.1.37; Phosphotyrosine, 21820-51-9; Protein-Tyrosine-Phosphatase, EC 3.1.3.48; Proto-Oncogene Proteins pp60(c-src), EC 2.7.1.112; Pyrazoles; Pyrimidines; Receptors, Calcitriol 
040 |a Scopus  |b spa  |c AR-BaUEN  |d AR-BaUEN 
030 |a JCEBD 
100 1 |a Capiati, D.A. 
245 1 0 |a Inhibition of serum-stimulated mitogen activated protein kinase by 1α,25(OH)2-vitamin D3 in MCF-7 breast cancer cells 
260 |c 2004 
270 1 0 |m Boland, R.L.; Dept. Biología, Bioquímica y Farmacia, Universidad Nacional del Sur, San Juan 670, 8000 Bahía Blanca, Argentina; email: rboland@criba.edu.ar 
506 |2 openaire  |e Política editorial 
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520 3 |a 1α,25-Dihydroxyvitamin D3 [1α,25(OH) 2D3], the hormonally active form of vitamin D3, has been shown to be a potent negative growth regulator of breast cancer cells both in vitro and in vivo. 1α,25(OH)2D3 acts through two different mechanisms. In addition to regulating gene transcription via its specific intracellular receptor (vitamin D receptor, VDR), 1α,25(OH) 2D3 induces rapid, non-transcriptional responses involving activation of transmembrane signal transduction pathways, like growth factors and peptide hormones. The mechanisms that mediate the antiproliferative effects of 1α,25(OH)2D3 in breast cancer cells are not fully understood. Particularly, there is no information about the early non-genomic signal transduction effectors modulated by the hormone. The present study shows that 1α,25(OH)2D3 rapidly inhibits serum induced activation of ERK-1 and ERK-2 MAP kinases. The tyrosine kinase Src is involved in the pathway leading to activation of ERK 1/2 by serum. Furthermore, 1α,25(OH)2D3 increases the tyrosine-phosphorylated state of Src and inhibits its kinase activity, while induces the association of the VDR with Src, either in the presence or absence of serum. In parallel, the hormone rapidly increases the amounts of VDR associated to plasma membranes (PM). Pretreatment with the tyrosine phosphatase inhibitors orthovanadate or bpV (phen) prevented mitogen-activated protein kinase (MAPK) inhibition by 1α,25(OH)2D3. These data altogether suggest that 1α,25(OH)2D3 inhibits the MAPK cascade by inactivating Src tyrosine kinase through a mechanism mediated by the VDR and tyrosine phosphatases. © 2004 Wiley-Liss, Inc.  |l eng 
593 |a Instituto de Ingeniería Genética y Biología Molecular, Vuelta de Obligado 2490, 1428 Buenos Aires, Argentina 
593 |a Departamento de Biología, Bioquímica y Farmacia, Universidad Nacional del Sur, San Juan 670, 8000 Bahía Blanca, Argentina 
593 |a Dept. Biología, Bioquímica y Farmacia, Universidad Nacional del Sur, San Juan 670, 8000 Bahía Blanca, Argentina 
690 1 0 |a 1Α,25(OH)2D3 
690 1 0 |a BREAST CANCER CELLS 
690 1 0 |a MAP KINASE 
690 1 0 |a SRC 
690 1 0 |a TYROSINE PHOSPHATASES 
690 1 0 |a VDR 
690 1 0 |a CALCITRIOL 
690 1 0 |a GROWTH FACTOR 
690 1 0 |a MITOGEN ACTIVATED PROTEIN KINASE 
690 1 0 |a MITOGEN ACTIVATED PROTEIN KINASE 1 
690 1 0 |a MITOGEN ACTIVATED PROTEIN KINASE 3 
690 1 0 |a ORTHOVANADIC ACID 
690 1 0 |a PEPTIDE HORMONE 
690 1 0 |a PROTEIN TYROSINE KINASE 
690 1 0 |a VITAMIN D RECEPTOR 
690 1 0 |a 4 AMINO 5 (4 METHYLPHENYL) 7 (TERT BUTYL)PYRAZOLO(3,4 D)PYRIMIDINE 
690 1 0 |a 4-AMINO-5-(4-METHYLPHENYL)-7-(TERT-BUTYL)PYRAZOLO(3,4-D)PYRIMIDINE 
690 1 0 |a CALCITRIOL RECEPTOR 
690 1 0 |a ENZYME INHIBITOR 
690 1 0 |a MITOGEN ACTIVATED PROTEIN KINASE 
690 1 0 |a PHOSPHOTYROSINE 
690 1 0 |a PROTEIN KINASE P60 
690 1 0 |a PROTEIN TYROSINE PHOSPHATASE 
690 1 0 |a PYRAZOLE DERIVATIVE 
690 1 0 |a PYRIMIDINE DERIVATIVE 
690 1 0 |a ARTICLE 
690 1 0 |a CELL MEMBRANE 
690 1 0 |a CELL STRAIN MCF 7 
690 1 0 |a DRUG INHIBITION 
690 1 0 |a ENZYME ACTIVITY 
690 1 0 |a HUMAN 
690 1 0 |a PRIORITY JOURNAL 
690 1 0 |a SIGNAL TRANSDUCTION 
690 1 0 |a TRANSCRIPTION REGULATION 
690 1 0 |a BREAST TUMOR 
690 1 0 |a CELL NUCLEUS 
690 1 0 |a CELL PROLIFERATION 
690 1 0 |a DRUG ANTAGONISM 
690 1 0 |a DRUG EFFECT 
690 1 0 |a ENZYME ACTIVATION 
690 1 0 |a ENZYMOLOGY 
690 1 0 |a METABOLISM 
690 1 0 |a PHOSPHORYLATION 
690 1 0 |a PROTEIN BINDING 
690 1 0 |a PROTEIN TRANSPORT 
690 1 0 |a SERUM 
690 1 0 |a TUMOR CELL LINE 
690 1 0 |a BREAST NEOPLASMS 
690 1 0 |a CALCITRIOL 
690 1 0 |a CELL LINE, TUMOR 
690 1 0 |a CELL MEMBRANE 
690 1 0 |a CELL NUCLEUS 
690 1 0 |a CELL PROLIFERATION 
690 1 0 |a ENZYME ACTIVATION 
690 1 0 |a ENZYME INHIBITORS 
690 1 0 |a HUMANS 
690 1 0 |a MITOGEN-ACTIVATED PROTEIN KINASES 
690 1 0 |a PHOSPHORYLATION 
690 1 0 |a PHOSPHOTYROSINE 
690 1 0 |a PROTEIN BINDING 
690 1 0 |a PROTEIN TRANSPORT 
690 1 0 |a PROTEIN-TYROSINE-PHOSPHATASE 
690 1 0 |a PROTO-ONCOGENE PROTEINS PP60(C-SRC) 
690 1 0 |a PYRAZOLES 
690 1 0 |a PYRIMIDINES 
690 1 0 |a RECEPTORS, CALCITRIOL 
690 1 0 |a SERUM 
690 1 0 |a SIGNAL TRANSDUCTION 
700 1 |a Rossi, A.M. 
700 1 |a Picotto, G. 
700 1 |a Benassati, S. 
700 1 |a Boland, R.L. 
773 0 |d 2004  |g v. 93  |h pp. 384-397  |k n. 2  |p J. Cell. Biochem.  |x 07302312  |t Journal of Cellular Biochemistry 
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856 4 0 |u https://hdl.handle.net/20.500.12110/paper_07302312_v93_n2_p384_Capiati  |y Handle 
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