DPY19L3 promotes vasculogenic mimicry by its C-mannosyltransferase activity

被引:1
作者
Baydoun, Hassan [1 ]
Kato, Yuji [1 ]
Kamo, Hiroki [1 ]
Huesch, Anna [1 ,2 ]
Mizuta, Hayato [1 ]
Kawahara, Ryota [1 ]
Simizu, Siro [1 ]
机构
[1] Keio Univ, Fac Sci & Technol, Dept Appl Chem, Yokohama 2238522, Japan
[2] Univ Tubingen, Fac Sci, Dept Pharm & Biochem, D-72074 Tubingen, Germany
关键词
C-mannosylation; Vasculogenic mimicry; MANNOSYLATION; BREAST; GLYCOSYLATION; CARCINOMA; SECRETION; MECHANISM; PROTEIN; DPY-19; CELLS;
D O I
10.32604/or.2023.030304
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
C-mannosylation is a post-translational modification that occurs intracellularly in the endoplasmic reticulum.In humans, biosynthesis ofC-mannosylation in proteins containing thrombospondin type 1 repeat is catalyzed by theDPY19 family; nonetheless, biological functions of proteinC-mannosylation are not yet fully understood, especially intumor progression. Vasculogenic mimicry (VM) is the formation offluid-conducting channels by highly invasive andgenetically deregulated tumor cells, enabling the tumors to form matrix-embedded vasculogenic structures, containingplasma and blood cells to meet the metabolic demands of rapidly growing tumors. In this study, we focused onDPY19L3, aC-mannosyltransferase, and aimed to unravel its role in VM. Knockout ofDPY19L3inhibited theformation of VM in HT1080 humanfibrosarcoma cells. Re-expression of wild-type DPY19L3 recovered VMformation; however, DPY19L3 isoform2, an enzymatic activity-defect mutant, did not restore it, suggesting that theC-mannosyltransferase activity of DPY19L3 is crucial to its function. Furthermore, the knockdown ofDPY19L3inMDA-MB-231 breast cancer cells hindered its network formation ability. Altogether, ourfindings suggest thatDPY19L3 is required for VM formation and stipulate the relevance ofC-mannosylation in oncogenesis
引用
收藏
页码:607 / 614
页数:8
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