Cell adhesion molecule 2 inhibits colorectal cancer progression through attenuating epithelial-mesenchymal transition

: Analysis of colorectal cancer (CRC) data revealed that cell adhesion molecule 2 (CADM2) is lowly expressed in tumor tissues. This study, therefore, aimed to elucidate the anti-oncogenesis roles of CADM2. The expression level CADM2 in The Cancer Genome Atlas (TCGA) were analyzed. We validated the expression level in adjacent normal, tumor, and metastatic tissues through real-time polymerase chain reaction (PCR) and immunohistochemistry (IHC). Methylation-specific PCR was used to explore the reason for the low expression. The biological function of CADM2 was verified by analyzing CCK-8 and transwell in cell line. Bioinformatics and Western blot analyses were used to explore anti-tumor progression pathways and the differences in immune infiltration levels. We found that CADM2 is weakly expressed in the TCGA and has good diagnostic performance. The low expression of CADM2 in cell lines and tissues was confirmed, and the hypoexpression was correlated with promoter hypermethylation. The IHC showed statistically significant decreased expression in primary focal compared to adjacent normal tissue, which further reduced in metastatic foci compared with primary foci. Up-regulation of CADM2 inhibited the growth and migrative and invasive ability of cells. When CADM2 expression was up-regulated, significant changes occurred in the expression of epithelialmesenchymal transition (EMT)-related protein. Bioinformatics analysis indicated that the molecular mechanism of CADM2 inhibiting tumor progression may also be related to the EMT process. Moreover, the CADM2 high-expression subgroup had higher immunity scores and infiltration levels. The research showed the association of CADM2 with carcinogenesis and metastasis by EMT process, providing new insight for molecular therapy and diagnosis of CRC.