Abstract
Cell-cell interactions and cell adhesion are key mediators of cancer progression and facilitate hallmarks of cancer including immune evasion and metastatic dissemination. Many cell adhesion molecules within the tumor microenvironment are changed and significant alterations of glycosylation are observed. These changes in cell adhesion molecules alter the ability of tumor cells to interact with other cells and extracellular matrix proteins. Three families of cell-cell interaction molecules selectins, Siglecs, and integrins have been associated with cancer progression in many pre-clinical studies, yet inhibition of cell adhesion as a therapeutic target is just beginning to be explored. We review how cell-cell interactions mediated by integrins and the glycan-binding receptors selectins and Siglec receptors support cancer progression. The discussion focuses on mechanisms during immune evasion and metastasis that can be therapeutically targeted by blocking these cell-cell interactions.
Highlights
Cancer progression induces immune evasion and eventually metastasis, a process consisting of several steps enabling tumor cells to leave the primary tumor, to intravasate and survive in the circulation, to extravasate and seed in distant organs and to initiate growth of metastatic lesions
We have found that tumorinfiltrating lymphocytes (TILs) upregulate different inhibitory CD33-related sialic acid-binding immunoglobulin-like lectins (Siglecs), predominantly Siglec-9 in patients with non-small cell lung cancer, colorectal cancer, epithelial ovarian cancer and melanoma [51, 52]
Alterations in cell adhesion and cell-cell interactions of tumor cells are inherently linked to many processes associated with immune evasion and metastasis that go beyond the scope of this review
Summary
Cancer progression induces immune evasion and eventually metastasis, a process consisting of several steps enabling tumor cells to leave the primary tumor, to intravasate and survive in the circulation, to extravasate and seed in distant organs and to initiate growth of metastatic lesions. Tumor cell interactions with other cells in the environment contribute to immune evasion and metastasis at every step of this process. On any cell, mediate interactions with other cells and the extracellular matrix in the microenvironment [1, 2]. Several families of cell adhesion molecules including cadherins, integrins, junctional-adhesion molecules, and selectins are altered during tumorigenesis. This mini review addresses the role of.
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