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Abstract Title:

Curcumin inhibits cell cycle progression of immortalized human umbilical vein endothelial (ECV304) cells by up-regulating cyclin-dependent kinase inhibitor, p21WAF1/CIP1, p27KIP1 and p53.

Abstract Source:

Int J Oncol. 2002 Aug;21(2):379-83. PMID: 12118335

Abstract Author(s):

Myung-Jin Park, Eun-Hee Kim, In-Chul Park, Hyung-Chan Lee, Sang-Hyeok Woo, Jae-Young Lee, Young-Joon Hong, Chang Hun Rhee, Seung-Hoon Choi, Bum-Sang Shim, Seung-Hoon Lee, Seok-Il Hong

Article Affiliation:

Laboratory of Cell Biology, Korea Cancer Center Hospital, 139-706 Seoul, Korea.

Abstract:

To elucidate possible mechanisms of anti-angiogenic activity by curcumin, we performed cDNA microarray and found that curcumin modulated cell cycle related gene expression. For further confirmation, DNA contents and expression levels of cyclins, cyclin-dependent kinases (CDKs), and CDK inhibitors (CDKIs) were examined by FACS analysis and Western blotting, respectively. Curcumin was found to induce G0/G1 and/or G2/M phase cell cycle arrest, up-regulate CDKIs, p21WAF1/CIP1, p27KIP1, and p53, and slightly down-regulate cyclin B1 and cdc2 in ECV304 cells. However, expression level of other cyclins and CDKs were not changed by curcumin. We, therefore, conclude that the up-regulation of CDKIs by curcumin plays a critical role in the regulation of cell cycle distribution in these cells, which may have a major role in anti-angiogenic activity of curcumin.

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Sayer Ji
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