Transcriptional activation of collagenase-3 by transforming growth factor-β1 is via MAPK and Smad pathways in human breast cancer cells

Nagarajan Selvamurugan; Ziawei Fung; Nicola C. Partridge

doi:10.1016/S0014-5793(02)03620-7

Transcriptional activation of collagenase-3 by transforming growth factor-β1 is via MAPK and Smad pathways in human breast cancer cells

Nagarajan Selvamurugan, Ziawei Fung, Nicola C. Partridge

Basic Science and Craniofacial Biology

Research output: Contribution to journal › Article › peer-review

Abstract

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.

Original language	English (US)
Pages (from-to)	31-35
Number of pages	5
Journal	FEBS Letters
Volume	532
Issue number	1-2
DOIs	https://doi.org/10.1016/S0014-5793(02)03620-7
State	Published - Dec 4 2002

Keywords

Breast cancer metastasis
Collagenase-3
Extracellular matrix
Transforming growth factor-β1 signaling

ASJC Scopus subject areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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title = "Transcriptional activation of collagenase-3 by transforming growth factor-β1 is via MAPK and Smad pathways in human breast cancer cells",

abstract = "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.",

keywords = "Breast cancer metastasis, Collagenase-3, Extracellular matrix, Transforming growth factor-β1 signaling",

author = "Nagarajan Selvamurugan and Ziawei Fung and Partridge, {Nicola C.}",

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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.

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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