Abstract
Chemokine receptor-ligand interactions are important to support functioning of both normal and pathologic cells. The expression and function of chemokine receptors in epithelial ovarian carcinoma (EOC) is largely unknown. Here, we report that the lymphotactin receptor (XCR1) was expressed in primary and metastatic human epithelial ovarian carcinoma (EOC) specimens and cell lines. In contrast, expression of XCR1 was not detected in the normal ovary or in human normal ovarian surface epithelial cells. Our data indicate that XCL1 and XCL2 are either present in the malignant ascites or expressed by the ovarian carcinoma cells. The addition of lymphotactin (XCL1 and XCL2) stimulated migration and proliferation of XCR1-positive cells. Reduction of XCR1 expression in ovarian carcinoma cell line SKOV-3 resulted in abrogated diaphragm and peritoneal wall tumor formation and in reduced frequency of colonic, splenetic, and liver nodules in an in vivo xenograft mouse model. Taken together, our data suggest that XCR1 is expressed early during the course of tumorigenic transformation and contributes towards increased cell migration and proliferation, which can facilitate the prometastatic behavior of EOC cells.
Highlights
Epithelial ovarian carcinoma (EOC) has a low incidence compared with other common cancers, with approximately 22,000 women diagnosed with epithelial ovarian carcinoma (EOC) annually
The current study investigated whether XCR1 was expressed in human specimens of EOC and whether it may have any functional significance in the progression of this disease
We tested for the expression of XCR1 in human specimens and cells from the normal ovary, normal ovarian surface epithelium (NOSE), normal immortalized ovarian surface epithelium, borderline EOC, primary EOC, and metastatic EOC by real-time PCR, immunohistochemistry, flow cytometry, and Western blot analysis
Summary
Epithelial ovarian carcinoma (EOC) has a low incidence compared with other common cancers, with approximately 22,000 women diagnosed with EOC annually. It is the leading cause of death from gynecologic malignancies and the fifth leading cause of cancer death in women, as over 14,000 patients succumb to this malignancy each year [1]. Current treatments are not effective against EOC once it reaches the late metastatic stages. Management of the metastatic disease becomes a crucial problem for the treatment of EOC. One possible way to resolve this problem is to target metastasis-specific pathways with novel therapies. Focused identification of novel target pathways and molecules that play a role in metastasis progression could
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
