Anti-gicerin IgG Reduces Adhesion, Wound Closure and Post-seeding Tumor Burden in T24 Bladder Carcinoma Models

Background/Aim: Gicerin, also termed HEMCAM in avian systems, is homologous to human melanoma cell adhesion molecule (MCAM), also known as CD146/MUC18. We examined whether an in-house rabbit polyclonal immunoglobulin G (IgG) raised against the tag-free extracellular domain of human MCAM/CD146, historically termed anti-gicerin IgG, reduces adhesion, migration-related wound closure and post-seeding tumor-burden endpoints in T24 bladder carcinoma cells. Materials and Methods: Antibody reactivity was examined by western blotting and immunofluorescence. Functional effects were assessed using MCAM/CD146-coated well adhesion, scratch wound-closure and coated-filter passage/retention assays, together with a tail-vein model in which antibody treatment began one day after tumor-cell injection and an intraperitoneal inoculation model in BALB/c nude mice. Results: The immune IgG, but not matched pre-immune IgG, recognized an approximately 120-kDa immunoreactive protein in T24-cell, mouse-lung and mouse-mesentery membrane fractions. Anti-gicerin IgG reduced adhesion in five independent matched experiments and reduced percentage wound closure and the number of cells recovered on the lower surface of coated filters in five independent matched experiments. In vivo, anti-gicerin IgG reduced post-seeding pulmonary tumor burden and post-seeding mesenteric nodule burden. Conclusion: The in-house anti-gicerin IgG reduced adhesion, migration-related wound closure and post-seeding tumor-burden endpoints in the T24 bladder carcinoma cells. Independent validation of MCAM/CD146 target specificity and the mechanisms underlying these effects is warranted.