N-glycosylated SGK196 suppresses the metastasis of basal-like breast cancer cells

Ci Xu; Meichao Zhang; Lei Bian; Yanyan Li; Yuan Yao; Dong Li

doi:10.1038/s41389-019-0188-1

N-glycosylated SGK196 suppresses the metastasis of basal-like breast cancer cells

Oncogenesis. 2020 Jan 8;9(1):4. doi: 10.1038/s41389-019-0188-1.

Authors

Ci Xu¹, Meichao Zhang¹, Lei Bian¹, Yanyan Li¹, Yuan Yao², Dong Li³

Affiliations

¹ Department of Radiation Oncology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
² Department of Radiation Oncology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China. yaoyuan@shsmu.edu.cn.
³ Department of Radiation Oncology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China. lidong@shsmu.edu.cn.

Abstract

SGK196 is a protein O-mannose kinase involved in an indispensable phosphorylation step during laminin-binding glycan synthesis on alpha-dystroglycan (α-DG). However, the function of SGK196 in cancer diseases remains elusive. In the current study, we demonstrated that SGK196 is primarily modified by N-glycosylation in breast cancer (BC) cells. Furthermore, gain and loss-of-function studies showed that N-glycosylated SGK196 suppresses cell migration, invasion, and metastasis in BC, particularly in the basal-like breast cancer (BLBC) type. In addition, we found that SGK196 N-glycosylation performs the regulatory function through the PI3K/AKT/GSK3β signaling pathway. Collectively, our results show that N-glycosylated SGK196 plays suppression roles in BLBC metastases, therefore providing new insights into SGK196 function in BC.