Decreased Synthesis of Matrix Metalloproteinase-7 and Adhesion to the Extracellular Matrix Proteins of Human Colon Cancer Cells Treated with Troglitazone

Surgery Today ◽  
2002 ◽  
Vol 32 (4) ◽  
pp. 343-350 ◽  
Author(s):  
Eiji Sunami ◽  
Nelson Hirokazu Tsuno ◽  
Joji Kitayama ◽  
Shinsuke Saito ◽  
Takuya Osada ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Extracellular Matrix ◽  
Matrix Metalloproteinase ◽  
Cancer Cells ◽  
Human Colon ◽  
Matrix Proteins ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Matrix Metalloproteinase 7 ◽  
Human Colon Cancer Cells

scholarly journals Syndecan-2 Functions as a Docking Receptor for Pro-matrix Metalloproteinase-7 in Human Colon Cancer Cells

2009 ◽  
Vol 284 (51) ◽  
pp. 35692-35701 ◽  
Author(s):  
Heui-Young Ryu ◽  
Jiseon Lee ◽  
Sanghwa Yang ◽  
Haein Park ◽  
Sojoong Choi ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Matrix Metalloproteinase ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Matrix Metalloproteinase 7 ◽  
Human Colon Cancer Cells

scholarly journals Acetylcholine-induced activation of M3 muscarinic receptors stimulates robust matrix metalloproteinase gene expression in human colon cancer cells

2009 ◽  
Vol 296 (4) ◽  
pp. G755-G763 ◽  
Author(s):  
Guofeng Xie ◽  
Kunrong Cheng ◽  
Jasleen Shant ◽  
Jean-Pierre Raufman
Keyword(s):  
Colon Cancer ◽  
Growth Factor ◽  
Matrix Metalloproteinase ◽  
Cancer Cells ◽  
Gene Transcription ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Egfr Ligand ◽  
Human Colon Cancer Cells

Previously, we showed that ACh-induced proliferation of human colon cancer cells is mediated by transactivation of epidermal growth factor (EGF) receptors (EGFRs). In the present study, we elucidate the molecular mechanism underlying this action. ACh-induced proliferation of H508 colon cancer cells, which express exclusively M3 muscarinic receptors (M3Rs), was attenuated by anti-EGFR ligand binding domain antibody, a broad-spectrum matrix metalloproteinase (MMP) inhibitor, anti-MMP7 antibody, a diphtheria toxin analog that blocks release of an EGFR ligand [heparin-binding EGF-like growth factor (HBEGF)], and anti-HBEGF antibody. Conditioned media from ACh-treated H508 cells induced proliferation of SNU-C4 colon cancer cells that express EGFR but not M3R. These actions were attenuated by an EGFR inhibitor and by anti-EGFR and anti-HBEGF antibodies. In H508, but not SNU-C4, colon cancer cells, ACh caused a striking dose- and time-dependent increase in levels of MMP7 mRNA and MMP7 protein. Similarly, ACh induced robust MMP1 and MMP10 gene transcription. ACh-induced MMP1, MMP7, and MMP10 gene transcription was attenuated by atropine, anti-EGFR antibody, and chemical inhibitors of EGFR and ERK activation. In contrast, inhibitors of phosphatidylinositol 3-kinase and NF-κB activation did not alter MMP gene transcription. Collectively, these findings indicate that MMP7-catalyzed release of HBEGF mediates ACh-induced transactivation of EGFR and consequent proliferation of colon cancer cells. ACh-induced activation of EGFR and downstream ERK signaling also regulates transcriptional activation of MMP7, thereby identifying a novel feed-forward mechanism for neoplastic cell proliferation.

Leptin is a growth factor for human colon cancer cells

2001 ◽  
Vol 120 (5) ◽  
pp. A493-A493
Author(s):  
J HARDWICK ◽  
G VANDENBRINK ◽  
S VANDEVENTER ◽  
M PEPPELENBOSCH
Keyword(s):  
Colon Cancer ◽  
Growth Factor ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells
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