FPR2 enhances colorectal cancer progression by promoting EMT process.

Formyl peptide receptor-2 (FPR2) has been shown to promote various tumors, but its role in colorectal cancer (CRC) has not been clearly illuminated. The aim of this study was to investigate the effect of FPR2 interference on cell proliferation, migration, invasion, apoptosis, pro-angiogenesis of CRC cells, and also the mechanisms involved. Quantitative PCR assays were applied to assess the expression levels of FPR2 in CRC tissues. CRC cell line SW1116 was chosen to perform this study. We knocked down FPR2 gene by sh-RNA. Then, the cell proliferation was assayed by soft agar colony formation assay, the cell migration capacity was checked by wound healing assay, and cell invasion ability was detected by transwell assay. In addition, flow cytometric analysis was used to detect apoptosis, while endothelial tube formation assay was used to evaluate the effects of FPR2 on pro-angiogenesis in vitro. Tumorigenesis experiment in vivo was performed in nude mice. EMT-related proteins were studied by western blotting. Quantitative PCR demonstrated that FPR2 mRNA was highly expressed in the colorectal cancer tissues. SW1116 cells' capacities of proliferation, migration, invasion, anti-apoptosis and pro-angiogenesis were distinctly suppressed after silencing FPR2 in SW1116 by sh-RNA. Suppression FPR2 mRNA in SW1116 cells suppressed tumorigenicity in nude mice. The expression of proteins related to epithelial-mesenchymal transition (EMT) such as E-cadherin, N-cadherin, Snail, Slug and vimentin was changed after suppressing FPR2. In conclusion, our study demonstrated that FPR2 could promote CRC cells progression in vitro and in vivo that may relate to promoting EMT.