Aberrant glycosylation is a universal feature of cancer cells. Cancer progression is composed of a number of sequential events that promote tumor cells to grow, leave the original site and eventually metastasize to other organs. These steps include loss of contact inhibition, immune evasion and crossing blood vessels. Glycan changes in malignant cells take a variety of forms and they appear to play important roles in each of these steps. Studies suggested that shortening O-glycans alone might be sufficient to induce cancerous transformation to enhance tumor growth and invasion. Upregulation of sialoglycans on cancer cells can inhibit immune response by binding to Siglecs on immune cells. Sialyl Lewis antigens bind selectins on platelets in the blood and endothelial cells of blood vessels to facilitate cancer cells to metastasize to distant sites, which is the leading cause of death.
This Research Topic aims to collect original research papers and review articles that further decipher the relationship between altered glycosylation and cancer progression. The Topic will be focused on the genetic mutations that lead to aberrant glycosylation in cancer cells, altered glycans identified in different tumors, and the molecular mechanisms by which aberrant glycans promote tumor growth and invasion. Cell surface glycans are sensed by glycan-binding receptors on immune cells, such as sialic acid binding immunoglobulin-type lectins (Siglecs) and C-type lectin receptors (CLRs). Similar to the role of PD1-PD-L1 interaction, the sialic acid-Siglec axis also functions as an inhibitory immune checkpoint. It is well known that a high percentage of cancer cells express shortened O-glycans, such T, Tn and STn antigens. The macrophage galactose-type lectin (MGL) has an exclusive specificity for terminal GalNAc structures such as Tn antigen. Previous work has suggested that the MGL-Tn interaction can function as an immune checkpoint. This Topic will emphasize the role of glycan-binding receptors in immune evasion and the development of novel drugs to interrupt the signaling pathways.
This collection welcomes Original Research, Review, Mini Review and Perspective on the interactions between tumor-associated glycan and their receptors on immune cells, and their roles in cancer growth and invasion. Areas of interest could include, but not limited to:
• Genetic mutations that lead to aberrant glycosylation in cancer cells;
• Functions of tumor-associated glycans in cancer development and progression;
• Roles of glycan-binding receptors such as Siglecs and CLRs in immune evasion;
• Development of antibody therapeutics targeting tumor-associated glycans;
• Development of antibody therapeutics targeting glycan-binding receptors on immune cells.
Keywords:
glycans, Glycosylation, Glycoscience, Tumor, Microenvironment
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Aberrant glycosylation is a universal feature of cancer cells. Cancer progression is composed of a number of sequential events that promote tumor cells to grow, leave the original site and eventually metastasize to other organs. These steps include loss of contact inhibition, immune evasion and crossing blood vessels. Glycan changes in malignant cells take a variety of forms and they appear to play important roles in each of these steps. Studies suggested that shortening O-glycans alone might be sufficient to induce cancerous transformation to enhance tumor growth and invasion. Upregulation of sialoglycans on cancer cells can inhibit immune response by binding to Siglecs on immune cells. Sialyl Lewis antigens bind selectins on platelets in the blood and endothelial cells of blood vessels to facilitate cancer cells to metastasize to distant sites, which is the leading cause of death.
This Research Topic aims to collect original research papers and review articles that further decipher the relationship between altered glycosylation and cancer progression. The Topic will be focused on the genetic mutations that lead to aberrant glycosylation in cancer cells, altered glycans identified in different tumors, and the molecular mechanisms by which aberrant glycans promote tumor growth and invasion. Cell surface glycans are sensed by glycan-binding receptors on immune cells, such as sialic acid binding immunoglobulin-type lectins (Siglecs) and C-type lectin receptors (CLRs). Similar to the role of PD1-PD-L1 interaction, the sialic acid-Siglec axis also functions as an inhibitory immune checkpoint. It is well known that a high percentage of cancer cells express shortened O-glycans, such T, Tn and STn antigens. The macrophage galactose-type lectin (MGL) has an exclusive specificity for terminal GalNAc structures such as Tn antigen. Previous work has suggested that the MGL-Tn interaction can function as an immune checkpoint. This Topic will emphasize the role of glycan-binding receptors in immune evasion and the development of novel drugs to interrupt the signaling pathways.
This collection welcomes Original Research, Review, Mini Review and Perspective on the interactions between tumor-associated glycan and their receptors on immune cells, and their roles in cancer growth and invasion. Areas of interest could include, but not limited to:
• Genetic mutations that lead to aberrant glycosylation in cancer cells;
• Functions of tumor-associated glycans in cancer development and progression;
• Roles of glycan-binding receptors such as Siglecs and CLRs in immune evasion;
• Development of antibody therapeutics targeting tumor-associated glycans;
• Development of antibody therapeutics targeting glycan-binding receptors on immune cells.
Keywords:
glycans, Glycosylation, Glycoscience, Tumor, Microenvironment
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.