Proteomic analysis of the molecular mechanism of curcumin/β-cyclodextrin polymer inclusion complex inhibiting HepG2 cells growth.

Abstract

This research aimed to explore whether curcumin/β-cyclodextrin polymer (CUR/CDP) inclusion complex caused inhibitory effect on HepG2 cells proliferation and its possible molecular mechanisms. We found that CUR/CDP inclusion complex exhibited inhibitory effects on HepG2 cells growth. To understand the underlying mechanism of how CUR/CDP inclusion complex inhibited HepG2 cells growth, we examined the proteome of HepG2 cells treated at 640\xa0μg/ml CUR/CDP inclusion complex using proteomic approach. We found that 15 protein spots identified by MALDI-TOF/TOF MS were changed. Biological progress analysis demonstrated that protein related to cell cycle and apoptosis accounted for 33% of the detected proteins. Among these proteins, nucleophosmin (NPM1) and peroxiredoxin-6 (PRDX6) were involved in the ROS-P53 pathway. PRDX6 and NPM1 were down-regulated, thereby improving the expression level of phosphorylated p53 and ROS content, which regulated cell apoptosis. This findings provide a better understanding of CUR/CDP regulatory anti-tumor mechanisms. PRACTICAL APPLICATIONS: Cyclodextrins polymer was used to prepare the curcumin/cyclodextrins polymer inclusion complex to improve curcumin solubility and stability in our group. And we found that it showed novel anticancer activity. However, the molecular mechanisms is unclear. This research elucidates the underlying molecular mechanisms of the curcumin/cyclodextrins polymer inclusion complex-inhibited HepG2 cells growth. The inclusion complex has the potential to be a novel complex of curcumin to treat human cancers.