FUT2 promotes the tumorigenicity and metastasis of colorectal cancer cells via the Wnt/β‑catenin pathway.

Abstract

The incidence of colorectal cancer (CRC), a leading cause of cancer‑related mortality, has increased globally. Fucosyltransferase 2 (FUT2), catalyzing the α1, 2‑linked fucose in mammals, has been reported to be overexpressed in several malignant cancers, including CRC. However, the effects of FUT2 on CRC remain largely unknown. Herein, it was determined that the FUT2 expression levels in CRC tissues were higher than those in adjacent non‑tumor tissues, whereas no association with tumor stage was revealed. The results of biological functional analysis revealed that FUT2 knockdown inhibited the proliferation, migration and invasion of human CRC cells. Moreover, the knockdown of FUT2 arrested the CRC cells at the G0/G1 phase and promoted the apoptosis of human CRC cells. Western blot analysis demonstrated that the expression levels of β‑catenin, C‑myc and cyclin D1 were decreased by FUT2 knockdown in CRC cells, whereas the expression of glycogen synthase kinase‑3β and the phosphorylation levels of β‑catenin were increased. Additionally, Wnt2 was fucosylated by FUT2 in CRC cells. Furthermore, the knockdown of FUT2 inhibited the growth of human CRC invivo. Overall, the findings of the present study suggest that FUT2 may be used as a potential diagnostic biomarker and therapeutic target for CRC treatment.