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Xiong et al. J Cancer Metastasis Treat 2016;2:357-64 Journal of
DOI: 10.20517/2394-4722.2016.08
Cancer Metastasis and Treatment
www.jcmtjournal.com
Review Open Access
Function of cancer cell-derived
extracellular matrix in tumor progression
Gao-Feng Xiong , Ren Xu 1,2
1
1 Markey Cancer Center, Lexington, KY 40536, USA.
2 Department of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY 40536, USA.
Correspondence to: Dr. Ren Xu, Department of Pharmacology and Nutritional Sciences, University of Kentucky, BBSRB, 741 S. Limestone,
Lexington, KY 40536, USA. E-mail: ren.xu2010@uky.edu
How to cite this article: Xiong GF, Xu R. Function of cancer cell-derived extracellular matrix in tumor progression. J Cancer Metasta Treat
2016;2:357-64.
Dr. Ren Xu is an Associated Professor at the Markey Cancer Center, University of Kentucky. Research in his
group focuses on the biological function and regulation of ECM microenvironment in normal tissue and cancer
development. His recent findings reveal the crucial function of cancer-cell derived-ECM in breast cancer progression.
ABSTRACT
Article history: Extracellular matrix (ECM) is an essential component of the tumor microenvironment.
Received: 18-02-2016 Cancer development and progression are associated with increased ECM deposition
Accepted: 06-07-2016 and crosslink. The chemical and physical signals elicited from ECM are necessary for
Published: 18-09-2016 cancer cell proliferation and invasion. It is well recognized that stromal cells are a major
source of ECM proteins. However, recent studies showed that cancer cells are also an
Key words: active and important component in ECM remodeling. Cancer cells deposit a significant
Tumor microenvironment, amount of collagen, fibronectin, and tenascin C (TNC). Recent studies demonstrate that
extracellular matrix, these cancer cell-derived ECM proteins enhance cancer cell survival and promote cancer
cancer progression, cell colonization at distant sites. ECM-related enzymes and chaperone proteins, such as
metastasis prolyl-4-hydroxylase, lysyl-hydroxylase, lysyl oxidase, and heat shock protein 47, are also
highly expressed in cancer cells. Inhibition of these enzymes significantly reduces cancer
growth, invasion, and metastasis. These factors suggest that the cancer cell-derived ECM
is crucial for cancer progression and metastasis. Therefore, targeting these ECM proteins
and ECM-related enzymes is a potential strategy for cancer treatment.
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