Syndecan-1 serves as a marker for the progression of epithelial ovarian carcinoma

Syndecan-1 (SDC-1) promotes the proliferation of cancer cells and plays a role in angiogenesis by binding to a variety of extracellular effectors. The present study was designed to compare the expression of SDC-1 in the normal ovary and in ovarian tumors, to better understand its roles in the progression of epithelial ovarian carcinoma (EOC).

The expression of SDC- 1, fibroblast growth factor 2 (FGF-2), and FGF receptor 1 (FGFRI) and their transcripts in 65 samples including the normal ovary, benign tumors, borderline ovarian tumors, and EOC was assessed using immunohistochemistry and the reverse transcription-polymerase chain reaction. The influence of FGF-2 on the expression of SDC-1 mRNA syndecan-1 in a human ovarian carcinoma cell line was determined using an FGF-2-neutralizing antibody.

SDC-l was not detected in normal ovarian tissue but was present in the epithelial cells of benign or borderline tumors and in ovarian adenocarcinomas. The levels of expression were significantly different in ovarian tissues derived from benign or malignant cases. Coordinate stromal expression of SDC-1 and its mRNA was detected at the original site of the tumor, as well as in metastatic foci in the greater omentum of ovarian adenocarcinomas. FGF-2 reduced the level of expression of SDC-1 mRNA when added exogenously to SKOV3 cells. This effect was abolished in the presence of an FGF-2-neutralizing antibody.

SDC-l contributes to the role of FGF-2 in proliferation and angiogenesis but may also play a role in the invasive properties of EOC. To the present authors' knowledge, this study is the first to report the presence of distinct patterns ofexpression of SDC-1 in local and metastatic foci in the greater omentum in patients with EOC. These data reinforce the role of the tumor stroma in the invasive properties of ovarian adenocarcinoma and suggest that stromal changes in the expression of SDC-1 may originate from the stroma and contribute to the pathogenesis and metastatic potential of EOC.