Abstract
Epithelial ovarian cancer (EOC) is the fifth leading cause of overall cancer death among American women. In 2010, 15,520 deaths were directly attributed to EOC; and 21,650 additional cases were diagnosed. When EOC is diagnosed prior to metastatic dissemination, the overall 5 year survival rate is 93%; however, over 75% of women with EOC are diagnosed with metastasis already present, dropping the survival rate to less than 20%. The process of EOC metastasis is unique in that epithelial cells detach from the primary tumor and shed into the peritoneal cavity as single cells and multicellular aggregates (MCA), which adhere intraperitoneally and invade the interstitial collagen-rich submesothelial matrix, where they proliferate to anchor secondary lesions. Proteolytic activity promotes the migration and collagen invasion crucial to metastatic success. Also key to cell migratory activity are focal adhesions (FA), integrin- and protease-rich cell adhesion sites that physically link the actin cytoskeleton to the extracellular matrix (ECM) and transduce signals into the intracellular compartment. Sites of adhesive contacts with collagen fibers have been associated with beta-1 integrin clustering and various matrix metalloproteinases. Membrane type 1 matrix metalloproteinase (MT1-MMP), an ECM degrading protease localized to the cell surface, has been shown to promote a collagen-invasive phenotype in ovarian carcinomas. Additionally, collagen-activated integrin-linked kinase (ILK), a beta-1 integrin cytoplasmic domain interactor, has been shown to regulate several biological processes that promote invasion and suppress anoikis. As initial steps to assess the contributions and potential inter-relationships of tumor cell invasion at FAs, presented here is a characterization of MT1-MMP and ILK expression in select ovarian cancer cell lines and in human EOC tumor tissue microarrays.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2459. doi:1538-7445.AM2012-2459
- ©2012 American Association for Cancer Research
Volume 72, Issue 8 Supplement
