Lung Tumor Cells with Different Tn Antigen Expression Present Distinctive Immunomodulatory Properties
Lung cancer is the first leading cause of cancer-related deaths in the world. Aberrant glycosylation in lung tumors leads to the expression of tumor-associated carbohydrate structures, such as the Tn antigen, consisting of N-acetyl-galactosamine (GalNAc) linked to a serine or threonine residue in pr...
| Authors: | , , , , , , , , , |
|---|---|
| Format: | article |
| Status: | Published version |
| Publication Date: | 2022 |
| Country: | Uruguay |
| Institution: | Universidad de la República |
| Repository: | COLIBRI |
| Language: | English |
| OAI Identifier: | oai:colibri.udelar.edu.uy:20.500.12008/54622 |
| Online Access: | https://hdl.handle.net/20.500.12008/54622 |
| Access Level: | Open access |
| Keyword: | Lung cancer Tn antigen Macrophage galactose-type lectin ¨Dendritic cells O-glycosylation NEOPLASIAS PULMONARES MACRÓFAGOS GALECTINAS ANTÍGENOS CÉLULAS DENDRÍTICAS GLICOSILACIÓN ACETILGALACTOSAMINA |
| Summary: | Lung cancer is the first leading cause of cancer-related deaths in the world. Aberrant glycosylation in lung tumors leads to the expression of tumor-associated carbohydrate structures, such as the Tn antigen, consisting of N-acetyl-galactosamine (GalNAc) linked to a serine or threonine residue in proteins (α-GalNAc-O-Ser/Thr). The Tn antigen can be recognized by the Macrophage Galactose/GalNAc lectin (MGL), which mediates various immune regulatory and tolerogenic functions, mainly by reprogramming the maturation of function of dendritic cells (DCs). In this work, we generated two different Tn-expressing variants from the Lewis-type lung murine cancer cell line LL/2, which showed different alterations in the O-glycosylation pathways that influenced the interaction with mouse MGL2 and the immunomodulatory properties of DCs. Thus, the identification of the biological programs triggered by Tn+ cancer cells might contribute to an improved understanding of the molecular mechanisms elicited by MGL-dependent immune regulatory circuits. |
|---|