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Intercellular adhesion molecule 2 (ICAM-2), also known as CD102, is a transmembrane glycoprotein and a member of the immunoglobulin superfamily that is constitutively expressed on vascular endothelial cells, platelets, and certain leukocyte subsets [1, 2]. It serves as a primary ligand for the integrin lymphocyte function-associated antigen-1 (LFA-1), mediating the stable adhesion and transendothelial migration of leukocytes during the immune response [4]. In oncology, ICAM-2 is recognized as a metastasis suppressor, particularly in neuroblastoma, where its high expression correlates with improved patient outcomes and reduced tumor cell migration [3]. Conversely, ICAM-2 has been implicated in promoting angiogenesis and cell survival in other contexts, highlighting its complex role in disease progression [1]. While there are currently no FDA-approved drugs that specifically target ICAM-2 mRNA or the protein itself, it remains a subject of intense research for RNA-based therapeutic strategies aimed at modulating its expression to treat cancer and inflammatory conditions [3].
Modulation of ICAM-2 expression or function to regulate leukocyte trafficking and tumor metastasis through interaction with LFA-1.
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