Abstract 2472: Peritoneal mechanobiology and metastatic success in epithelial ovarian cancer

Abstract

Abstract Less than 30% of women diagnosed with epithelial ovarian cancer (EOC) survive for 5 years due to metastatic disease. EOC progression is accompanied by accumulation of ascites (up to 4 liters), changing intraperitoneal (i.p.) fluid pressure from subatmospheric (-5 mmHg) to >20 mmHg with tense ascites. The overall consequence of altered peritoneal mechanobiology on EOC metastatic success is currently unknown. Due to altered i.p. fluid dynamics the peritoneal mesothelium, an elastic soft tissue, may be modified by exposure to tensional force (strain). Mechanical strain (stretching) on intact murine mesothelial explants causes increased tissue stiffness, as determined by atomic force microscopy, and enhances ovarian tumor cell adhesion. To approximate the compressive force environment on EOC cells in tense ascites, cells were seeded in suspension in polystyrene bags and cultured under a compressive load (Instron, 25mmHg, 8h). Increased fluid pressure enhances proliferation in multiple cell lines and increases expression of N-cadherin, a mesenchymal marker, in Dov13 cells. These data suggest that ascites-induced changes in peritoneal mechanobiology may potentiate EOC metastatic success. Support: NIH-R01CA109545, NIH R01CA086984, NIH F31 R01CA086984-12S1. 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 2472. doi:1538-7445.AM2012-2472