Advanced ovarian cancers contain 2 distinct phenotypic populations: (a) free-floating tumor cells in the ascitic fluid and (b) solid tumors. Ascites cells are derived from the solid tumors and spread throughout the peritoneum. Changes in cell-cell and cell-extracellular matrix interactions are thought to be responsible for the origin of ascites cells. Since E-cadherin molecules play a crucial role in the cell-cell interactions in epithelial cells, we investigated the expression of E-cadherin in these 2 phenotypic populations. Paired samples of ascites and solid tumors were obtained from patients. Both primary tumors and tumor cells isolated from an experimental model showed a marked decrease in E-cadherin expression in the ascites cells compared to the respective solid tumors. Semi-quantitative, reverse transcriptase-polymerase chain reaction (RT-PCR) was used to determine the steady-state levels of E-cadherin-specific mRNA. Results indicate that the primary tumors had significantly lower levels of E-cadherin transcript in ascites cells when compared to their solid tumor counterparts. Changes in E-cadherin expression were also reflected in the invasion capacity of tumor cells in vitro. Ascites cells were 4-fold more invasive then solid tumor cells, suggesting that ascites cells are a highly malignant phenotype.
Transplantation of the human ovarian adenocarcinoma cell line, NIH:OVCAR-3 into athymic mice produces two morphologically distinct tumor cell populations (ascites and solid tumors). In the present study, we isolated both tumor cell phenotypes and investigated their relative malignant potential. Since cytoskeletal and morphological changes correlate with metastatic phenotype, expression of the intermediate-filament protein vimentin was compared between ascites and solid tumors. Ascites tumor cells showed a less differentiated epithelial morphology and concurrently expressed higher levels of vimentin. Ascites cells were more efficient in anchorage independent growth when compared with their solid tumor counterpart. Ascites tumor cells were also highly motile compared with the solid tumor cell population (P = 0.006). Migration of ascites tumor cells was further enhanced by type IV collagen, hyaluronic acid, and chondroitin sulfate A. Solid tumor cells removed from the same animal, however, were not significantly affected by these agents. From these studies, we conclude that ovarian cancer cells present in ascites are phenotypic variants which are highly motile compared with solid tumor cells isolated from the same animal. Ascites tumor cells with increased motility may contribute to peritoneal seeding and metastasis.
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