Icam1, also known as Intercellular adhesion molecule 1 or CD54, is a cell surface glycoprotein in the immunoglobulin supergene family. It serves as an adhesion receptor regulating leukocyte recruitment to inflammation sites. ICAM1 interacts with lymphocyte function-associated antigen 1 (LFA-1) and macrophage 1-antigen (Mac-1) receptors, and its expression is regulated by the NF-κB signaling pathway. It plays a crucial role in various biological processes including inflammation, injury resolution, and tumorigenesis [3,6].

Depletion of ICAM1 in TNBC cells abrogates lung colonization by inhibiting homotypic tumor cell-tumor cell cluster formation, and blocking ICAM1 interactions significantly inhibits CTC cluster formation, tumor cell transendothelial migration, and lung metastasis, suggesting it can be a therapeutic target for TNBC metastasis [1]. In colorectal cancer, Fusobacterium nucleatum enhances CRC cells' adhesion to endothelial cells, promotes extravasation and metastasis by inducing ICAM1 expression through the ALPK1/NF-κB axis [2]. In TNBC, ICAM1 promotes bone metastasis via integrin-mediated TGF-β/EMT signaling, and silencing ICAM1 expression inhibits bone metastasis in mice [4]. In gastric cancer stem cells, knockout of ICAM1 (GCSC-ICAM1KO) leads to loss of migration, invasion, and metastasis capabilities [5].

In conclusion, ICAM1 is a key regulator in multiple biological processes. Through gene knockout-based studies in various cancer models, it has been shown to play a significant role in cancer metastasis, highlighting its potential as a therapeutic target in cancer treatment. These model-based research findings contribute to a better understanding of the mechanisms underlying disease progression related to ICAM1.