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Fucosyltransferase VII promotes proliferation via the EGFR/AKT/mTOR pathway in A549 cells

Authors Liang J, Gao W, Cai L

Received 2 May 2017

Accepted for publication 26 June 2017

Published 7 August 2017 Volume 2017:10 Pages 3971—3978

DOI https://doi.org/10.2147/OTT.S140940

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Akshita Wason

Peer reviewer comments 3

Editor who approved publication: Dr Samir Farghaly

Jin-xiao Liang,1 Wei Gao,2 Lei Cai1

1Department of Thoracic Surgery, Zhejiang Cancer Hospital, 2School of Medicine, Zhejiang University City College, Hangzhou, People’s Republic of China

Abstract: Fucosyltransferase VII (FUT7) is one of a1,3-fucosyltransferases family that catalyzes the final fucosylation step in the synthesis of Lewis antigens and generates a unique glycosylated product sialyl Lewis X (sLeX). sLeX can serve as ligands for E- or P-selectin expressed on the cell surface and results in cancer metastasis and angiogenesis. However, the molecular biological mechanisms of FUT7 elevation in neoplastic cells are still largely unknown. In this study, we examined the impact of FUT7 on cell proliferation and migration in A549 cells by colony formation assay, cell cycle assay, gelatin zymography, wound-healing assay, transwell invasion assay and Western blot. In addition, we identified that FUT7 activated EGFR/AKT/mTOR signal pathway that correlated with sLeX augmentation. In conclusion, FUT7 overexpression augments sLeX synthesis to trigger cell proliferation via the activation of EGFR/AKT/mTOR signaling pathway, which indicated that FUT7 may be a potential therapeutic target for epithelial cancers with a high expression of FUT7 and sLeX.

Keywords: fucosyltransferase VII, epidermal growth factor receptor, lung cancer, proliferation, signal pathway

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