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Cell adhesion molecule 1 (CADM1), widely known as Tumor Suppressor in Lung Cancer 1 (TSLC1), is a transmembrane glycoprotein belonging to the immunoglobulin superfamily (UniProt Q9BY67). It functions primarily as a mediator of cell-cell adhesion through homophilic and heterophilic interactions, which are essential for maintaining tissue architecture and regulating intracellular signaling pathways that suppress oncogenic transformation (Kuramochi et al., 2001). In many solid tumors, such as lung, esophageal, and pancreatic cancers, the expression of CADM1 is frequently silenced by promoter hypermethylation, which facilitates tumor growth, invasion, and metastasis. Conversely, CADM1 is highly overexpressed in adult T-cell leukemia/lymphoma (ATLL), where it acts as a specific cell surface marker and contributes to the adhesion of leukemic cells to vascular endothelial cells (Sasaki et al., 2013). Therapeutic strategies targeting CADM1 often utilize gene therapy, where the TSLC1 transgene is delivered via viral vectors to restore tumor-suppressive activity and induce apoptosis in malignant cells (Mao et al., 2003). Beyond oncology, CADM1 is also involved in synapse formation and maintenance in the central nervous system, highlighting its diverse roles in cellular communication.
Restoration of tumor suppressor activity via gene replacement therapy, leading to the induction of caspase-dependent apoptosis and the inhibition of tumor cell migration and invasion.
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