NCAM and attached polysialic acid affect behaviors of breast epithelial cells through differential signaling pathways  

作　　者：Yurong Wu Juhong Yang Xin Wang Jia Guo Zengqi Tan Feng Guan Lin Cao 

机构地区：[1]Provincial Key Laboratory of Biotechnology,Joint International Research Laboratory of Glycobiology and Medicinal Chemistry,College of Life Sciences,Northwest University,Xi’an 710069,China [2]Shandong University of Arts,Ji’nan 250300,China [3]Institute of Biomedical Engineering and Health Sciences,Changzhou University,Changzhou 213164,China [4]Provincial Key Laboratory of Biotechnology,Joint International Research Laboratory of Glycobiology and Medicinal Chemistry,School of Medicine,Northwest University,Xi’an 710069,China

出　　处：《Acta Biochimica et Biophysica Sinica》2024年第11期1584-1593,共10页生物化学与生物物理学报(英文版)

基　　金：This work was supported by the grants from the National Natural Science Foundation of China(Nos.82172828 and 32271338);Science Foundation for Distinguished Young Scholars of Shaanxi Province(No.2021JC-39);the Natural Science Foundation of Shaanxi Province(No.2022JQ-205);Shaanxi Innovation Team Project(No.2023-CX-TD-58);Shaanxi Fundamental Science Research Project for Chemistry&Biology(Nos.22JHQ077 and 23JHQ042).

摘　　要：Neural cell adhesion molecule(NCAM),a common mammalian cell surface glycoprotein,is the major substrate of polysialic acid(polySia).Polysialylated NCAM occurs in many types of cancer,but rarely in normal adult tissues.The functional role of NCAM hypersialylation in the epithelial-mesenchymal transition(EMT)process remains unclear.The present study indicates that NCAM and attached polysialic acid affect behaviors of breast epithelial cells through differential signaling pathways.NCAM and polysialylated NCAM are aberrantly regulated in breast cancer cells.They are both upregulated in normal breast epithelial cells undergoing EMT.Western blot analysis demonstrates that NCAM-140 overexpression induces EMT in breast epithelial cells and promotes cell proliferation and migration through activation of theβ-catenin/slug signaling pathway.Modification of polySia attached to NCAM modulates cell adhesion and promotes cell motility through activation of the EGFR/STAT3 pathway.These observations contribute to clarifying the molecular mechanisms by which polysialic acid and its major substrate,NCAM,modulate cell behaviors,and highlight the significance of increased polysialylated expression on NCAM during EMT and tumor development.

关 键 词：neural cell adhesion molecule polysialic acid epithelial-mesenchymal transition β-catenin/slug EGFR/STAT3 

分 类 号：R737.9[医药卫生—肿瘤]