Background At least one-third of epithelial ovarian cancers are associated with the development of ascites containing heterogeneous cell populations, including tumor cells, inflammatory cells, and stromal elements. the epithelial type and mesenchymal type cells were 36 h and 48 h, respectively, indicating faster growth of the epithelial type cells compared to the mesenchymal type cells. Cultured in vitro, these ascitic cells displayed the potential for self-renewal and long-term proliferation, and expressed the typical cancer stem/progenitor cell markers CD44high, CD24low, and AC133+. These CA-074 Methyl Ester reversible enzyme inhibition cells also demonstrated high BMP-2, BMP4, TGF-, Rex-1, and AC133 early gene expression, and expressed EGFR, integrin 21, CD146, and Flt-4, which are highly associated with tumorigenesis and metastasis. The epithelial type cells demonstrated higher cytokeratin 18 and E-cadherin expression than the mesenchymal type cells. The mesenchymal type cells, in contrast, demonstrated higher AC133, CD73, CD105, CD117, EGFR, integrin 21, and CD146 surface marker expression than the epithelial type cells. Conclusion The established culture system provides an in vitro model for the selection of drugs that target cancer-associated stromal progenitor cells, and for the development of ovarian cancer treatments. strong class=”kwd-title” Keywords: human cancer initiating/stem cell, stromal progenitor cells, epithelial ovarian adenocarcinoma, epithelial-mesenchymal CA-074 Methyl Ester reversible enzyme inhibition transition Background Ovarian cancer is the fifth leading cause of death from cancer in the Western world, and the leading cause of death from gynecologic cancer. More than 90% CA-074 Methyl Ester reversible enzyme inhibition of ovarian cancers arise from the surface epithelium [1,2]. In Taiwan ovarian cancer is the tenth leading cause of female malignancy and the leading cause of death from gynecological cancer. Seventy-five percent of epithelial CA-074 Methyl Ester reversible enzyme inhibition ovarian cancer (EOC) patients receive a diagnosis at the advanced stage, and among these, at least one-third are associated with the development of ascites, an abnormal collection of exudate with a cellular fraction consisting mainly of cancer cells, lymphocytes, and mesothelial cells [3,4]. Efforts at improving the survival of CA-074 Methyl Ester reversible enzyme inhibition patients with EOC have focused on early detection and on the development of novel chemotherapeutic drugs. However, long-term survival of patients with Rabbit Polyclonal to p38 MAPK (phospho-Thr179+Tyr181) advanced ovarian cancer remains limited (below 20%). Understanding the mechanisms underlying the initiation and progression of ovarian cancer is therefore essential for the development of effective treatments. Components of ascites, including neoplastic cells and pro-angiogenic or tumorgenic factors, may contribute to the proliferation and spread of cancer cells . Results from previous investigations indicate that in addition to the neoplastic cancer cells, stromal cells that are heterogeneous and composed of fibroblasts, endothelial or methothelial cells, adipocytes or adipose tissue-derived stromal cells, bone marrow-derived stem cells, and immune cells promote tumor growth, invasion, and metastasis by cross-talk with cancerous cells [6,7]. Prior research has established that ascites commonly develops in patients with EOC, and that the presence of abnormal stromal cells in the ascites may establish an unusual microenvironment for tumor spreading. However, the roles of these abnormal stromal cells in the development of ovarian cancer remain poorly understood. Tumor development is mainly associated with the accumulation of multiple genetic and epigenetic alterations, resulting in the transformation of a normal cell to a cancer cell . The components of tumors are complex, comprising genetically or epigenetically altered tumor cells surrounded by a heterogeneous population of stromal cells. The cellular and molecular interactions between tumor and stromal cells trigger tumor growth and metastatic spreading . Increasing evidence has suggested that the growth capability of a tumor is dependent on cancer stem cells or cancer initiating cells (CSCs/CICs), which represent a minority of cells within tumors . Although investigators proposed the existence of CSCs/CICs several decades ago, it was not until 1997 that Bonnet et al. first isolated these cells from patients with acute myeloid leukemia . Further studies subsequently described the isolation of CICs from patients with prostate, melanoma, lung, colon, and pancreas cancer [12-16]. CICs may be derived from abnormal stem cells or from differentiated tumor.