The oncogenic role of the cerebral endothelial cell adhesion molecule (CERCAM) in bladder cancer cells in vitro and in vivo

Bladder cancer is a menace to global health worldwide due to its high recurrence rate and its progression to invasive muscular complications. Cell adhesion molecules play an intricate role in cancer migration, growth, and invasion. Therefore, through bioinformatics analysis, it was found that the higher cerebral endothelial cell adhesion molecule (CERCAM) predicted lower chance in bladder cancer patient survival; subsequently, in vitro and in vivo investigations were performed to evaluate the specific effects of CERCAM on bladder cancer cell phenotypes and tumor growth in mice model. The PCR-based analysis revealed an aberrant upregulation of CERCAM in bladder carcinoma tissues and cells when compared with normal controls. In vitro, functional experiments such as MTT, EdU, and Transwell assays showed that CERCAM overexpression markedly enhanced bladder cancer cell viability, DNA synthesis, and cell invasion. In contrast, CERCAM silencing suppressed bladder cancer cell viability, DNA synthesis, and cell invasion. CERCAM overexpression significantly increased PCNA, Vimentin, Twist, and N-cadherin proteins but decreased E-cadherin and cleaved-caspase3, whereas CERCAM silencing exerted opposite effects on these markers. In vivo, subcutaneous implant model experiments in nude mice showed that CERCAM silencing suppressed the growth of subcutaneously implanted tumors. CERCAM altered the phosphorylation process of AKT. The PI3K inhibitor LY294002 treatment manifested similar effects as CERCAM silencing on bladder cancer cell behaviors and partially impaired the promotive functions of CERCAM overexpression upon the capacity of bladder cancer cells to proliferate and invade. When taken together, the cell adhesion molecule CERCAM is overexpressed in bladder cancer tissues. In vitro, CERCAM overexpression significantly promoted bladder cancer cell viability, DNA synthesis, and cell invasion and alters the cleaved-caspase3, E-cadherin, and N-cadherin expression pattern; in vivo, CERCAM silencing suppressed tumor growth in nude mice. The PI3K/AKT signaling is suspected of interfering participate in the functions of CERCAM in bladder carcinoma.

Automated summary

The study revealed that CERCAM is overexpressed in bladder cancer, promoting cell growth and invasion. In vivo experiments showed that CERCAM silencing suppressed tumor growth. The PI3K/AKT signaling pathway may play a role in the functions of CERCAM in bladder carcinoma.