Additionally, our data showed that DNMT1 up-regulation induced by IL-6/STAT3 signaling was indispensable for IL-6-mediated hepaCAM loss in RCC cell lines ACHN and 769-P, while DNMT3b up-regulation was crucial for hepaCAM loss in A498.
To further investigate the reason for the low expression of hepaCAM in renal carcinoma and the corresponding molecular mechanisms, we detected renal carcinoma OS-RC-2 cell lines containing high expression of hepaCAM; and hepaCAM and p-AKT were also detected in these cells.
Our data show that hepaCAM is frequently downregulated in RCC, and that exogenous hepaCAM exhibits antiproliferative effect on 786-0 cells, suggesting that silencing of hepaCAM may be associated with carcinogenesis of RCC.