To understand the possible mechanism, we showed that the expression levels of downstream effectors, such as the anti-apoptosis index, proliferation index, index for a metabolic switch to aerobic glycolysis, angiogenesis indexes, and survival pathway index were reduced, suggesting that huMETCAM/MUC18 may mediate tumor suppression via elevated apoptosis and decreased anti-apoptosis, angiogenesis, proliferation, and metabolic switch to aerobic glycolysis. Here, MCAM is linked to neoplasm.