TY - JOUR
T1 - Transcriptional activation of collagenase-3 by transforming growth factor-β1 is via MAPK and Smad pathways in human breast cancer cells
AU - Selvamurugan, Nagarajan
AU - Fung, Ziawei
AU - Partridge, Nicola C.
N1 - Funding Information:
This research was supported by grants from the Department of Defense (DAMD17-01-1-0656), the New Jersey Commission on Cancer Research and the Foundation of the University of Medicine and Dentistry of New Jersey (to N.S.) and the National Institutes of Health DK47420 (to N.C.P.). We thank Drs. Carlos Lopez-Otin for providing human collagenase-3 cDNA and Riko Nishimura for human Smad3 mutant cDNA.
Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2002/12/4
Y1 - 2002/12/4
N2 - Transforming growth factor (TGF)-β1, a crucial molecule in metastatic bone cancer, stimulates collagenase-3 expression in the human breast cancer cell line, MDA-MB231. Cycloheximide inhibited this stimulation, indicating that de novo protein synthesis was essential for this response. We examined whether mitogen-activated protein kinase (MAPK) and/or Smad pathways are involved in TGF-β1-stimulated collagenase-3 expression in MDA-MB231 cells. Biochemical blockade of extracellular regulated kinase-1/2 and p38 MAPK pathways partially abolished TGF-β1-stimulated collagenase-3 mRNA expression; whereas overexpression of a dominant negative form of Smad3 completely blocked the TGF-β1-response. These data indicate that TGF-β1-induced MAPK and Smad pathways are involved in TGF-β1-stimulated collagenase-3 expression in MDA-MB231 cells.
AB - Transforming growth factor (TGF)-β1, a crucial molecule in metastatic bone cancer, stimulates collagenase-3 expression in the human breast cancer cell line, MDA-MB231. Cycloheximide inhibited this stimulation, indicating that de novo protein synthesis was essential for this response. We examined whether mitogen-activated protein kinase (MAPK) and/or Smad pathways are involved in TGF-β1-stimulated collagenase-3 expression in MDA-MB231 cells. Biochemical blockade of extracellular regulated kinase-1/2 and p38 MAPK pathways partially abolished TGF-β1-stimulated collagenase-3 mRNA expression; whereas overexpression of a dominant negative form of Smad3 completely blocked the TGF-β1-response. These data indicate that TGF-β1-induced MAPK and Smad pathways are involved in TGF-β1-stimulated collagenase-3 expression in MDA-MB231 cells.
KW - Breast cancer metastasis
KW - Collagenase-3
KW - Extracellular matrix
KW - Transforming growth factor-β1 signaling
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U2 - 10.1016/S0014-5793(02)03620-7
DO - 10.1016/S0014-5793(02)03620-7
M3 - Article
C2 - 12459458
AN - SCOPUS:0037021435
VL - 532
SP - 31
EP - 35
JO - FEBS Letters
JF - FEBS Letters
SN - 0014-5793
IS - 1-2
ER -