Formyl peptide receptor 2 expression predicts poor prognosis and promotes invasion and metastasis in epithelial ovarian cancer.

Formyl peptide receptor 2 (FPR2) has been identified as a member of the G protein-coupled chemoattractant receptor (GPCR) family and has been implicated as playing a role in both inflammation and cancer development. Epithelial ovarian cancer (EOC) has been suggested to be correlated with both infectious and non-infectious inflammation. To date, the role of FPR2 in EOC remains poorly understood and controversial. In the present study, we aimed to investigate the potential of FPR2 in regulating EOC. We performed immunohistochemistry and RT-qPCR to analyzed expression of FPR2 in EOC tissues and the correlation between FPR2 and EOC clinicopathological characteristics as well as prognosis were also analyzed. To test the role of FPR2 in EOC cell migration, we established FPR2-knockdown SKOV3 cells and performed wound-healing, Transwell and angiogenesis assays to detect the metastatic potential of these EOC cells. Our studies found that FPR2 was overexpressed in EOC tissues and was positively correlated with EOC clinicopathological characteristics including the International Federation of Gynecology and Obstetrics (FIGO) stage, histological grade and ovarian cancer type. Survival analyses suggested that FPR2 overexpression indicated the poorer prognosis of EOC patients and FPR2 may act as an independent risk factor for EOC prognosis. FPR2 knockdown decreased the migration potential of the ovarian cancer cells. Moreover, serum amyloid A (SAA) may stimulate the migration of SKOV3 cells through FPR2. The present study suggested that FPR2 promoted the invasion and metastasis of EOC and it could be a prognostic marker for EOC.