Nitidine chloride inhibits renal cancer cell metastasis via suppressing AKT signaling pathway

Abstract

Nitidine Chloride (NC) has been shown to have anti-cancer effects on various tumors. However, whether NC could exert anti-metastasis activity in renal cancer cells and the underlying mechanisms have not been elucidated. In this work, our data demonstrated the anti-metastasis effects of NC on renal cancer cells in vitro. With scratch assay and transwell assays, we found that NC potently suppressed the migration and invasion of 786-O and A498 cells. Mechanistically, we presented that NC significantly decreased phosphorylation of AKT, accompanied by down-regulation of MMP-2 and MMP-9. Furthermore, a specific AKT inhibitor, LY294002, could enhance the anti-metastasis effects of NC, which indicated that NC suppressed metastasis of renal cancer cells partly via inhibition of AKT activity. Taken together, our results imply that NC can be developed as a potential anti-metastasis agent to renal cancer.

Keywords: AKT; AKT/PKB; DMEM; DMSO; Dimethylsulfoxide; Dulbecco’s Modified Eagle’s Medium; FBS; Fetal Bovine Serum; MMP; Metastasis; Nitidine chloride; PBS; PBST; Phosphate Buffered Saline; Phosphate Buffered Saline and Tween 20; RAC-alpha serine/threonine-protein kinase; Renal cancer; matrix metalloproteinase.