Abstract 4325: Localization and expression of osteopontin in a chitosan-treated ovarian cancer cell line, SKOV-3

Abstract

Abstract Ovarian cancer is the deadliest gynecological malignancy and despite current treatments, such as chemotherapy and radiotherapy, reoccurrence of this deadly malignancy is high. Although elevated levels of osteopontin (OPN), a phosphorylated glycoprotein, are always present in the ovaries, recent studies have implicated osteopontin (OPN) protein as a novel biomarker for ovarian cancer. Early detection of ovarian cancer is imperative, and furthermore, novel treatments with fewer adverse effects than current treatments of chemotherapy and radiation, are currently being investigated. Chitosan, a natural polysaccharide that is biodegradable and biocompatible, may serve as a potential alternative treatment for ovarian cancer, and may function by regulating OPN expression. Therefore, the objective of this study was to determine the effects of chitosan on the expression and localization of OPN in SKOV-3 cells. It was hypothesized that the expression of OPN protein will be down-regulated in a dose-dependent manner. To test this hypothesis, SKOV-3 cells were treated with 0, 50, 100, 250, and 500, ng/mL of chitosan for 48 hours. An MTT assay was performed to determine cell viability and proliferation rate. Cells were harvested; total protein was isolated and then subjected to SDS-PAGE and Western blot analysis. The localization of OPN was determined using immunocytochemistry, after chitosan treatment of SKOV-3 cells on two-chamber slides for 48 hours. The expression of OPN decreased in SKOV-3 cells in a dose-dependent manner. In addition, cell proliferation tended to decrease with increasing dose of chitosan. These data indicate that chitosan may inhibit SKOV-3 cell proliferation by decreasing OPN production and secretion. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4325. doi:10.1158/1538-7445.AM2011-4325