Collagen Clinical Study

Barbolina MV, Adley BP, Ariztia EV, Liu Y, Stack MS.

Cell & Molecular Biology, Northwestern University, Chicago, IL 60611.

Late stage ovarian cancer is characterized by disseminated intraperitoneal metastasis as secondary lesions anchor in the type I and III collagen-rich submesothelial matrix. Ovarian carcinoma cells preferentially adhere to interstitial collagen, and collagen-induced integrin clustering upregulates the expression of the transmembrane collagenase membrane type 1 matrix metalloproteinase (MT1-MMP). Collagenolytic activity is important in intraperitoneal metastasis, potentiating invasion through the mesothelial cell layer and colonization of the submesothelial collagen-rich matrix. The objective of this study was to elucidate a potential mechanistic link between collagen adhesion and MT1-MMP expression. Our results indicate that culturing cells on 3-dimensional collagen gels, but not thin layer collagen or synthetic 3-dimensional hydrogels, results in rapid induction of the transcription factor Egr-1. Integrin signaling through a Src kinase-dependent pathway is necessary for Egr-1 induction. Silencing of Egr-1 expression using siRNA abrogated collagen-induced MT1-MMP expression and inhibited cellular invasion of 3-dimensional collagen gels. These data support a model for intraperitoneal metastasis wherein collagen adhesion and clustering of collagen binding integrins activates integrin-mediated signaling via Src kinases to induce expression of Egr-1, resulting in transcriptional activation of the MT1-MMP promoter and subsequent MT1-MMP-catalyzed collagen invasion. This model highlights the role of unique interactions between ovarian carcinoma cells and interstitial collagens in the ovarian tumor microenvironment in inducing gene expression changes that potentiate intraperitoneal metastatic progression.

PMID: 17158885 [PubMed - as supplied by publisher]

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