Calebin-A induces cell cycle arrest in human colon cancer cells and xenografts in nude mice. (October 2016)

• Record Type: Journal Article
• Authors: Liou, Wen-Shiung; Lin, Chen; Lee, Pei-Sheng; Kalyanam, Nagabhushanam; Ho, Chi-Tang; Pan, Min-Hsiung
• Is Part Of: Journal of functional foods. Volume 26(2016)
• Page Start: 781
• Page End: 791
• Publication Date: 2016-10
• Subjects: Calebin-A -- Cell cycle -- Colon cancer -- Curcuminoids -- Xenograft; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2016.08.047
• Languages: English
• ISSNs: 1756-4646

Abstract

Highlights: Calebin-A inhibited colon cancer cell growth and induced cell cycle arrest. Calebin-A markedly inhibited S and G2/M cell cycle regulatory proteins. Calebin-A significantly decreased tumour volumes and tumour sizes. Calebin-A may be useful as a cancer therapeutic and chemopreventive agent. Abstract: Calebin-A is a curcuminoid compound isolated from turmeric. Herein, we investigated the antiproliferative effect of calebin-A in human colon cancer cells and demonstrated that calebin-A had a more potent inhibition on cell growth compared with curcumin and tetrahydrocurcumin. In this study, calebin-A caused G2 /M cycle arrest through decreasing the protein levels of cdc25A, cyclin B, cyclin A and cdc2 and increasing cyclin-dependent kinases inhibitors (CDKI) such as p53 and p21. Moreover, calebin-A increased reactive oxygen species (ROS) levels, triggered a DNA damage response and up-regulated the phosphorylation of H2 AX, chk1, chk2. Furthermore, intraperitoneally administrated calebin-A on HCT116 tumour xenografts in vivo significantly decreased tumour volumes as well as reduced tumour sizes and proliferating cell nuclear antigen (PCNA) protein levels. These results have an important implication for using calebin-A as a functional food ingredient for cancer prevention.