2. Academic Validation
  3. N-glycosylation of Siglec-15 decreases its lysosome-dependent degradation and promotes its transportation to the cell membrane

N-glycosylation of Siglec-15 decreases its lysosome-dependent degradation and promotes its transportation to the cell membrane

  • Biochem Biophys Res Commun. 2020 Nov 26;533(1):77-82. doi: 10.1016/j.bbrc.2020.08.111.
Xiaojian Chen 1,  Xuening Dang 1,  Jinglue Song 1,  Guanghui Wang 2,  Chenying Liu 1,  Long Cui 3,  Zhenyu Huang 4
Affiliations

Affiliations

  • 1 Department of Colorectal and Anal Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, PR China.
  • 2 Guizhou Provincial People's Hospital Guiyang, Guizhou, PR China.
  • 3 Department of Colorectal and Anal Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, PR China. Electronic address: cuilong@xinhuamed.com.cn.
  • 4 Department of Colorectal and Anal Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, PR China. Electronic address: huangzyu@outlook.com.
PMID: 32921411 DOI: 10.1016/j.bbrc.2020.08.111
Abstract

Siglec-15 was recently reported to be an immunosuppressive molecule that is expressed by tumor-associated macrophages and upregulated in some solid tumors. Targeting Siglec-15 is a potential strategy for normalization Cancer Immunotherapy. Here, we identified the important post-translational modification, N-glycosylation of Siglec-15, which is regulated by glucose uptake. Using a series of glycosidase and glycosylation inhibitors, we demonstrated that Siglec-15 was completely N-glycosylated in vitro and in vivo. The precise glycosylation site was determined. N-glycosylation stabilized Siglec-15 by decreasing its lysosome-dependent degradation. Siglec-15 subcellular distribution detected by immunofluorescence indicated that N-glycosylation promoted Siglec-15 transportation to the cell membrane. The collective observations indicate that targeting the N-glycosylation of Siglec-15 may be an effective supplement to immunotherapy.

Keywords

Lysosome-dependent degradation; N-Glycosylation; Siglec-15; Subcellular distribution.

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