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Epithelial cell adhesion molecule (EpCAM), which is expressed in the majority of epithelial tissues, exhibits tumor growth promoting abilities and is overexpressed in human epithelial ovarian cancer. Therefore, EpCAM is considered to be a promising target for specific immune‑based therapies. The present study evaluated the role of IL‑6 and IL‑8 in the expression of EpCAM in the A2780 human ovarian cancer cell line. Furthermore, the cellular localization of the EpCAM protein in A2780 cells was determined and the effect of EpCAM inhibition on the proliferation of the A2780 cells was investigated. An MTT assay demonstrated that blocking EpCAM with anti‑EPCAM antibodies had no effect on cellular metabolic activity (proliferation). Gene expression analysis revealed that IL‑8 increased EpCAM expression, whereas IL‑6 and the combination of IL‑6/IL‑8 had no effect on EpCAM expression. Immunofluorescence analysis confirmed that EpCAM is expressed on A2780 cell membranes. The present results demonstrated that IL‑8 increased EpCAM expression at the mRNA level in ovarian cancer cells and suggested a potential role of IL‑6 as an inhibitor of IL‑8‑stimulated EpCAM expression.

The aim of the present study was to assess the role of interleukin (IL)‑6 and IL‑8 on the expression of fluid‑phase complement inhibitor, factor H (FH), and FH‑like protein 1 (FHL‑1), in the A2780 ovarian carcinoma cell line. This cell line does not normally produce IL‑6, however, is IL‑6 responsive due to the presence of receptor for IL‑6. The presence of FH and FHL‑1 in the cell lysates was confirmed by western blotting. The levels of FH and FHL‑1 in the medium were determined by enzyme‑linked immunosorbent assay. To evaluate gene expression, reverse transcription‑quantitative polymerase chain reaction was performed. The cellular localization of FH and FHL‑1 in ovarian cancer cells was assessed by immunofluorescence. The present study revealed that FH, contrary to FHL‑1, was secreted by ovarian cancer cells, however, this process was independent of IL stimulation. No significant differences were observed in the concentration of FH in the control cells, when compared with the samples treated with IL‑6/IL‑8. The results of western blotting revealed that the protein expression levels of FH and FHL‑1 were not regulated by IL‑6 and IL‑8 in a dose‑dependent manner. Immunofluorescence analysis confirmed that the A2780 ovarian cancer cell line expressed both membrane bound and intracellular forms of FH and FHL‑1. The present data revealed that the A2780 cells expressed and secreted FH protein and are also able to bind FH and FHL‑1. This may influence the efficiency of complement mediated immunotherapy.