Journal
MOLECULAR CANCER RESEARCH
Volume 10, Issue 1, Pages 11-24Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1541-7786.MCR-11-0256
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Funding
- NIH [1R21CA160917]
- NATIONAL CANCER INSTITUTE [R21CA160917] Funding Source: NIH RePORTER
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Epithelial ovarian carcinoma (EOC) is a deadly disease, and little is known about the mechanisms underlying its metastatic progression. Using human specimens and established cell lines, we determined that the G-protein-coupled seven-transmembrane fractalkine receptor (CX(3)CR1) is expressed in primary and metastatic ovarian carcinoma cells. Ovarian carcinoma cells robustly migrated toward CX(3)CL1, a specific ligand of CX3CR1, in a CX(3)CR1-dependent manner. Silencing of CX3CR1 reduced migration toward human ovarian carcinoma ascites fluid by approximately 70%. Importantly, adhesion of ovarian carcinoma cells to human peritoneal mesothelial cells was dependent on CX(3)CL1/CX(3)CR1 signaling. In addition, CX3CL1 was able to induce cellular proliferation. Together, our data suggest that the fractalkine network may function as a major contributor to the progression of EOC, and further attention to its role in the metastasis of this deadly malignancy is warranted. Mol Cancer Res; 10(1); 11-24. (C) 2011 AACR.
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