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

FEBS Letters

Fung, Ziawei¹  Partridge, Nicola C¹  Selvamurugan, Nagarajan¹ 

[1] Department of Physiology and Biophysics, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, 675 Hoes Lane, Piscataway, NJ 08854, USA

关键词: Extracellular matrix;    Collagenase-3;    Transforming growth factor-β1 signaling;    Breast cancer metastasis;    MMP;    matrix metalloproteinase;    TGF-β1;    transforming growth factor-β1;    ECM;    extracellular matrix;    PTH;    parathyroid hormone;    PTHrP;    parathyroid hormone-related protein;    RT-PCR;    reverse transcription polymerase chain reaction;    MAPK;    mitogen-activated protein kinase;    ERK;    extracellular signal-regulated kinase;   

DOI  :  10.1016/S0014-5793(02)03620-7

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown