| Abstract: |
C-type lectins, distinguished by a C-type lectin binding domain (CTLD), are an evolutionarily conserved superfamily of glycoproteins that are implicated in a broad range of physiologic processes. The group XIV subfamily of CTLDs are comprised of CD93, CD248/endosialin, CLEC14a, and thrombomodulin/CD141, and have important roles in creating and maintaining blood vessels, organizing extracellular matrix, and balancing pro- and anti-coagulative processes. As such, dysregulation in the expression and downstream signaling pathways of these proteins often lead to clinically relevant pathology. Recently, group XIV CTLDs have been shown to play significant roles in cancer progression, namely tumor angiogenesis and metastatic dissemination. Interest in therapeutically targeting tumor vasculature is increasing and the search for novel angiogenic targets is ongoing. Group XIV CTLDs have emerged as key moderators of tumor angiogenesis and metastasis, thus offering substantial therapeutic promise for the clinic. Herein, we review our current knowledge of group XIV CTLDs, discuss each’s role in malignancy and associated potential therapeutic avenues, briefly discuss group XIV CTLDs in the context of two other relevant lectin families, and offer future direction in further elucidating mechanisms by which these proteins function and facilitate tumor growth. © The Author(s) 2024. |
| Keywords: |
immunohistochemistry; osteosarcoma; signal transduction; epidermal growth factor; protein expression; unclassified drug; review; cancer growth; nonhuman; protein function; neoplasm; neoplasms; cd8+ t lymphocyte; enzyme inhibition; transforming growth factor beta; protein protein interaction; protein targeting; gelatinase b; protein binding; in vivo study; enzyme activation; in vitro study; pathology; angiogenesis; neovascularization, pathologic; tumor antigen; alpha smooth muscle actin; liver metastasis; th2 cell; immunotherapy; antigens, neoplasm; gamma interferon; glioblastoma; breast carcinoma; down regulation; upregulation; metastasis potential; th1 cell; antigens, cd; monocyte; tumor growth; macrophage; tumor vascularization; cell adhesion; hypoxia inducible factor 1alpha; focal adhesion kinase; neovascularization (pathology); g protein coupled receptor; leukocyte antigen; interleukin 12; enzyme mechanism; insulin like growth factor binding protein 7; somatomedin binding protein; fibrinogen; endothelial leukocyte adhesion molecule 1; thrombomodulin; padgem protein; tumor angiogenesis; high mobility group b1 protein; lectins, c-type; pericyte; epithelial mesenchymal transition; mouth squamous cell carcinoma; lectin; l selectin; proteinase activated receptor 1; c-type lectin; platelet derived growth factor bb; humans; human; complement component c1q receptor; activated protein c; endosialin; myeloid-derived suppressor cell; microvascular density; efferocytosis; endothelial protein c receptor; vessel normalization; beta dystroglycan; c type lectin family 14 member a; g protein coupled receptor 15; cd248 protein, human
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