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岩藻糖基转移酶VII通过EGFR/AKT/mTOR途径促进A549细胞增殖。

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

作者信息

Liang Jin-Xiao, Gao Wei, Cai Lei

机构信息

Department of Thoracic Surgery, Zhejiang Cancer Hospital.

School of Medicine, Zhejiang University City College, Hangzhou, People's Republic of China.

出版信息

Onco Targets Ther. 2017 Aug 7;10:3971-3978. doi: 10.2147/OTT.S140940. eCollection 2017.

DOI:10.2147/OTT.S140940
PMID:28860805
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5558582/
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 (sLe). sLe 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 sLe augmentation. In conclusion, FUT7 overexpression augments sLe 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 sLe.

摘要

岩藻糖基转移酶VII（FUT7）是α1,3-岩藻糖基转移酶家族的成员之一，它催化Lewis抗原合成中的最后一步岩藻糖基化反应，并产生独特的糖基化产物唾液酸化Lewis X（sLe）。sLe可作为细胞表面表达的E-选择素或P-选择素的配体，导致癌症转移和血管生成。然而，肿瘤细胞中FUT7升高的分子生物学机制仍不清楚。在本研究中，我们通过集落形成试验、细胞周期试验、明胶酶谱分析、伤口愈合试验、Transwell侵袭试验和蛋白质印迹法，研究了FUT7对A549细胞增殖和迁移的影响。此外，我们发现FUT7激活了与sLe增加相关的EGFR/AKT/mTOR信号通路。总之，FUT7过表达通过激活EGFR/AKT/mTOR信号通路增加sLe合成以触发细胞增殖，这表明FUT7可能是FUT7和sLe高表达的上皮癌的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17fa/5558582/f5bf8fa7e14f/ott-10-3971Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17fa/5558582/ccb92e1b76e5/ott-10-3971Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17fa/5558582/e5109ccae46b/ott-10-3971Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17fa/5558582/7912aa3d5dbc/ott-10-3971Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17fa/5558582/57258161d0b7/ott-10-3971Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17fa/5558582/f5bf8fa7e14f/ott-10-3971Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17fa/5558582/ccb92e1b76e5/ott-10-3971Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17fa/5558582/e5109ccae46b/ott-10-3971Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17fa/5558582/7912aa3d5dbc/ott-10-3971Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17fa/5558582/57258161d0b7/ott-10-3971Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17fa/5558582/f5bf8fa7e14f/ott-10-3971Fig5.jpg

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