Abstract: Objective To explore the effect of fibroblast growth factor 18 (FGF-18) in colon cancer. Methods The colon cancer cell lines (SW480) were cultured in vitro and divided into 3 groups: control group, shRNA-NC group and sh-FGF-18 group. The cells proliferation was detected by colony formation assay. The apoptosis was detected by flow cytometry. The changes of cells morphology after apoptosis were observed by Hoechst. The cell migration was detected by wound healing assay. The cell invasion was detected by Transwell assay. The metastasis of liver and lung tissues was observed by HE staining. The expression levels of epithelial-mesenchymal transition (EMT) related markers [ E-cadherin ( E-cad ), N-cadherin ( N-cad ), fibronectin ( FN)] were detected by Western blotting. The volume and size of tumors were detected by tumor formation assay in nude mice. The positive expressions of E-cad, N-cad and FN in colon cancer tissues were detected by immunohistochemistry. Results Compared with these in the shRNA-NC group, the relative expression levels of FGF-18 mRNA and protein were decreased in the FGF-18-shRNA group, the number of colonies, migrated cells and invasive cells were reduced, the number of apoptotic cells was increased, the expression level of E-cad was increased, and the expression levels of N-cad and FN were decreased. The positive rate of E-cad expression in colon cancer tissues in the sh-FGF-18 group was higher than that in the shRNA-NC group, while the positive rate of N-cad and FN expressions were lower than those in the shRNA-NC group (P< 0. 05). The tumor weight of primary lesions was lower, and the volume was smaller in the sh-FGF-18 group when compared with those in the shRNA-NC group (P< 0. 05), and there were fewer metastases of liver and lung tissues in the sh-FGF 18 group (P< 0. 05). Conclusion Interfering with FGF-18 can inhibit the proliferation, migration and invasion of colon cancer cells, promote apoptosis and inhibit xenograft growth in nude mice, which may affect tumors metastasis by inhibiting EMT pathway.

Key words: fibroblast growth factor 18, colon cancer, proliferation, anti-tumor