Tenascin-C upregulates matrix metalloproteinase-9 in breast cancer cells: direct and synergistic effects with transforming growth factor beta1
- PMID: 12672030
- DOI: 10.1002/ijc.11037
Tenascin-C upregulates matrix metalloproteinase-9 in breast cancer cells: direct and synergistic effects with transforming growth factor beta1
Abstract
Tenascin-C (TN-C) and matrix metalloproteinases (MMPs) are highly expressed in cancer tissues and probably promote cell migration during cancer progression. TN-C and MMPs are often co-localized in areas of active tissue remodeling in pathologic conditions, suggesting reciprocal regulation. To investigate whether TN-C regulates MMPs expression in cancer cells, we first exposed mammary cancer cells derived from TN-C-deficient mice to TN-C and examined MMPs expression. TN-C was then compared with fibronectin (FN), laminin (LN), basic fibroblast growth factor (b-FGF) and transforming growth factor-beta1 (TGF-beta1). Results of endpoint RT-PCR, quantitative real-time RT-PCR and gelatin zymography demonstrated that TN-C, strongly and dose dependently, upregulates MMP-9 expression in murine mammary cancer cells. TN-C weakly induced MMP-2, MMP-3 and MMP-13. FN and LN induced MMP-9 to lesser extents compared with TN-C. b-FGF had no effect on MMP-9 expression. TGF-beta1 induced MMP-9 expression in a dose-dependent manner, and this induction was significantly enhanced by addition of TN-C. TN-C and TGF-beta1 also upregulated MMP-9 expression in the human breast cancer cell line MDA-MB-231. Neutralization with specific anti-TGF-beta1 antibody showed decreased expression of MMP-9, indicating that TGF-beta controls the baseline MMP-9 expression by a direct autocrine mechanism. Under neutralization of TGF-beta, addition of TN-C still upregulated MMP-9. Conversely, neutralization of endogenous TN-C (in a TN-C-positive mammary cancer cell line) downregulated TGF-beta-induced MMP-9 expression. Thus, TN-C induces MMP-9 expression directly and by collaboration with TGF-beta. These findings reveal a novel role of TN-C in breast cancer progression.
Copyright 2003 Wiley-Liss, Inc.
Similar articles
-
Co-stimulation of human breast cancer cells with transforming growth factor-beta and tenascin-C enhances matrix metalloproteinase-9 expression and cancer cell invasion.Int J Exp Pathol. 2004 Dec;85(6):373-9. doi: 10.1111/j.0959-9673.2004.00406.x. Int J Exp Pathol. 2004. PMID: 15566434 Free PMC article.
-
[Interactions of ovarian carcinoma cells and human peritoneal mesothelial cells involved in matrix metalloproteinases expressions of ovarian carcinoma cells].Zhonghua Fu Chan Ke Za Zhi. 2006 Mar;41(3):194-7. Zhonghua Fu Chan Ke Za Zhi. 2006. PMID: 16640888 Chinese.
-
Expression of matrix metalloproteinases in cyclosporin-treated gingival fibroblasts is regulated by transforming growth factor (TGF)-beta1 autocrine stimulation.J Periodontol. 2002 Nov;73(11):1313-22. doi: 10.1902/jop.2002.73.11.1313. J Periodontol. 2002. PMID: 12479636
-
Glioma cell invasion: regulation of metalloproteinase activity by TGF-beta.J Neurooncol. 2001 Jun;53(2):177-85. doi: 10.1023/a:1012209518843. J Neurooncol. 2001. PMID: 11716069 Review.
-
Human odontoblast culture method: the expression of collagen and matrix metalloproteinases (MMPs).Adv Dent Res. 2001 Aug;15:55-8. doi: 10.1177/08959374010150011401. Adv Dent Res. 2001. PMID: 12640741 Review.
Cited by
-
Phase contrast microscopy analysis of breast tissue: differences in benign vs. malignant epithelium and stroma.Anal Quant Cytol Histol. 2009 Aug;31(4):197-207. Anal Quant Cytol Histol. 2009. PMID: 19736867 Free PMC article.
-
Shaping eosinophil identity in the tissue contexts of development, homeostasis, and disease.J Leukoc Biol. 2018 Jul;104(1):95-108. doi: 10.1002/JLB.1MR1117-442RR. Epub 2018 Apr 14. J Leukoc Biol. 2018. PMID: 29656559 Free PMC article. Review.
-
Tenascin-C regulates recruitment of myofibroblasts during tissue repair after myocardial injury.Am J Pathol. 2005 Jul;167(1):71-80. doi: 10.1016/S0002-9440(10)62954-9. Am J Pathol. 2005. PMID: 15972953 Free PMC article.
-
Tenascin-C: a novel mediator of hepatic ischemia and reperfusion injury.Hepatology. 2011 Dec;54(6):2125-36. doi: 10.1002/hep.24639. Hepatology. 2011. PMID: 21898491 Free PMC article.
-
Targeting ECM Disrupts Cancer Progression.Front Oncol. 2015 Oct 20;5:224. doi: 10.3389/fonc.2015.00224. eCollection 2015. Front Oncol. 2015. PMID: 26539408 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Miscellaneous