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Cosmc 转染通过改变 O-聚糖结构降低 Tn 细胞的恶性行为，并增强其对 Apo2L/TRAIL 诱导的细胞凋亡的敏感性。

Cosmc transfection decreases malignant behavior of Tn cells and enhances sensitivity to apoptosis when induced by Apo2L/TRAIL via alteration of O-glycan structure.

机构信息

Department of Immunology, Binzhou Medical University, Yantai 264003, PR China.

Qingdao University, Qingdao 266071, PR China.

出版信息

Aging (Albany NY). 2021 Oct 13;13(19):23393-23406. doi: 10.18632/aging.203633.

DOI:10.18632/aging.203633
PMID:34644263
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8549606/
Abstract

Cosmc mutations may cause abnormal O-glycosylation and result in Tn antigen expression. In the current study, it was discovered that proliferation and migration of Tn+ cells (Jurkat T and LS174T-Tn cells) with mutant Cosmc decreased after transfected Cosmc, and their sensitivity to apoptosis induced by Apo2L/TRAIL increased. Core 1-, 2-, and 3-derived O-glycans were absent in Tn cells. After Cosmc transfection, normal extended core 1-derived O-glycans appeared and were accompanied by increased T-synthase activity. Core 2-derived O-glycans appeared in transfected LS174T-Tn cells, and their structural types and levels were lower than those in LS174T-Tn cells. Core 3-derived O-glycans were present only in LS174T-Tn cells. The activity of C3GnT in LS174T-Tn cells was lower than that in LS174T-Tn cells, and it was absent in Jurkat T cells. Cosmc transfection did not alter C3GnT activity or core 3-derived O-glycans in Jurkat T and LS174T-Tn cells. The results demonstrated that the composition and structure of O-glycans were different among various Tn cells, which not only affected cell malignant behavior but also modulated sensitivity to apoptotic stimuli. Thus, Cosmc transfection may effectively decrease the malignant behavior of Tn tumor cells and enhance their sensitivity to apoptosis when induced by Apo2L/TRAIL through modification of O-glycans.

摘要

Cosmc 突变可能导致异常的 O-糖基化，并导致 Tn 抗原的表达。在本研究中，发现突变 Cosmc 转染后 Tn+细胞（Jurkat T 和 LS174T-Tn 细胞）的增殖和迁移减少，其对 Apo2L/TRAIL 诱导的细胞凋亡的敏感性增加。Tn 细胞中不存在核心 1-、2-和 3-衍生的 O-聚糖。转染 Cosmc 后，正常的扩展核心 1 衍生的 O-聚糖出现，并伴随着 T-合酶活性的增加。转染的 LS174T-Tn 细胞中出现了核心 2 衍生的 O-聚糖，其结构类型和水平低于 LS174T-Tn 细胞。LS174T-Tn 细胞中仅存在核心 3 衍生的 O-聚糖。LS174T-Tn 细胞中的 C3GnT 活性低于 LS174T-Tn 细胞，而 Jurkat T 细胞中则不存在。Cosmc 转染并未改变 Jurkat T 和 LS174T-Tn 细胞中的 C3GnT 活性或核心 3 衍生的 O-聚糖。结果表明，不同 Tn 细胞中 O-聚糖的组成和结构不同，这不仅影响细胞恶性行为，而且调节对凋亡刺激的敏感性。因此，Cosmc 转染可通过修饰 O-聚糖有效降低 Tn 肿瘤细胞的恶性行为，并增强其对 Apo2L/TRAIL 诱导的细胞凋亡的敏感性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56cd/8549606/33a30e83f2af/aging-13-203633-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56cd/8549606/af004d97f032/aging-13-203633-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56cd/8549606/8c6ab08c57d9/aging-13-203633-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56cd/8549606/70f6480880e9/aging-13-203633-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56cd/8549606/0d7db827c828/aging-13-203633-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56cd/8549606/33a30e83f2af/aging-13-203633-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56cd/8549606/af004d97f032/aging-13-203633-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56cd/8549606/8c6ab08c57d9/aging-13-203633-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56cd/8549606/70f6480880e9/aging-13-203633-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56cd/8549606/0d7db827c828/aging-13-203633-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/56cd/8549606/33a30e83f2af/aging-13-203633-g005.jpg

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