AKAP4 mediated tumor malignancy in esophageal cancer.

AKAP4 as a new Cancer/Testis (CT) antigen is expressed not only in human germ cells, but also expressed in various tumor cells. AKAP4 is correlated with tumor malignancy; however, the role of AKAP4 in esophageal cancer remains unknown. Here we explored the function of AKAP4 in esophageal cancer. We found that AKAP4 mRNA and protein levels were up-regulated in the esophageal cancer tissues compared to normal control. In KYSE150 cell line, inhibition of AKAP4 suppressed cell growth and invasiveness. Overexpression of AKAP4 promoted cell growth and invasiveness. In addition, expression of epithelial markers (E-cadherin and ZO-1) was up-regulated or down-regulated and expression of mesenchymal markers (vimentin and N-cadherin) was down-regulated or up-regulated after knockdown or overexpression of AKAP4 in vitro. In vivo in a xenograft model silencing AKAP4 suppressed tumor growth. We also found that NF-κB p65 bound to AKAP4 promoter and regulated expression of AKAP4. In conclusion, overexpression of AKAP4 is associated with esophageal cancer progression. Inhibition of AKAP4 leads to suppressed growth and invasion of esophageal cancer.