Epithelial ovarian cancer is the most lethal gynecologic malignancy with the majority of cases being diagnosed after the disease has become metastatic according to the report by Obstetrics and Gynecology, Duke University Medical Center USA, 2008.

Consequently, genetic and epigenetic changes that disturb motility are likely to be important for the pathogenesis of ovarian cancer. Although ovarian cancer can be cured in up to 90% of cases while still confined to the ovary, approximately 70% are diagnosed after the occurrence of peritoneal dissemination, when the cure rate reduces to less than 30% according to recent studies by Global Cancer Statistic, CA Cancer 2011.

Recent reports have shown 25% of most cancerous cells within tumors have the features of cancer stem cells (CSCs). CSCs have been identified on the basis of their ability to self-renew and to have the capacity to differentiate into cancer cells and also form tumors in animal model.

We already demonstrated that the majority of cells of ovarian cancer cell line (OVCAR) expressed CD133 and CD117 antigen. The CD133 antigen is a 120 kDa membrane glycoprotein, detected first time in CD34+ hematopoietic stem cells and thus this antigen has been widely used to identify and facilitate the isolation of hematopoietic stem and progenitor cells. CD117 or stem cell factor receptor (c-Kit), also detected in Haemopoietic stem and progenitor cells. This protein is a type 3 transmembrane receptor for MGF (mast cell growth factor).

CD133and CD117 has been considered as a marker of CSCs. Also OVCAR CD133- cells subpopulation in “in vitro” culture can generate a subpopulation of OVCAR CD133+ cells, probably via Epithelial to Mesenchymal Transition (EMT).

EMT describes a mechanism by which cells lose their epithelial characteristics and acquire more migratory mesenchymal properties. It also seems to have a key role in the acquisition of invasive and migratory properties in many types of carcinoma cells.

We aim to determine whether the transformation of these cancer cells in CSCs is dependent on the tumor type and on signaling pathways. We will be using genomic and proteomic analysis OVCAR CD133+/- and CD117+/- cells for targeting the EMT pathway.


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