Caffeic acid phenethyl ester induces E2F-1-mediated growth inhibition and cell-cycle arrest in human cervical cancer cells

doi:10.1111/febs.12242

CNU IR > College of Sustainable Environment and Recreation > Dept. of Recreation and Health-Care Management > Periodical Articles > Item 310902800/27788

Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/27788

Title:	Caffeic acid phenethyl ester induces E2F-1-mediated growth inhibition and cell-cycle arrest in human cervical cancer cells
Authors:	Hsu, Tzu-Hui Chu, Chin-Chen Hung, Mei-Whey Lee, Hwei-Jen Hsu, Hsien-Jun Chang, Tsu-Chung
Contributors:	休閒保健管理系
Keywords:	Apoptosis Caffeic Acid Phenethyl Ester Cell-Cycle Arrest Cervical Cancer Cells E2F-1 Factor
Date:	2013-06
Issue Date:	2014-05-26 10:43:42 (UTC+8)
Publisher:	Wiley-Blackwell
Abstract:	Caffeic acid phenyl ester (CAPE) has been identified as an active component of propolis, a substance that confers diverse activities in cells of various origins. However, the molecular basis of CAPE-mediated cellular activity remains to be clarified. Here, we show that CAPE preferentially induced S- and G2/M-phase cell-cycle arrests and initiated apoptosis in human cervical cancer lines. The effect was found to be associated with increased expression of E2F-1, as there is no CAPE-mediated induction of E2F-1 in the pre-cancerous cervical Z172 cells. CAPE also up-regulated the E2F-1 target genes cyclinA, cyclinE and apoptotic protease activating of factor1 (Apaf-1) but down-regulated cyclinB and induced myeloid leukemia cell differentiation protein (Mcl-1). These results suggest the involvement of E2F-1 in CAPE-mediated growth inhibition and cell-cycle arrest. Transient transfection studies with luciferase reporters revealed that CAPE altered the transcriptional activity of the apaf-1 and mcl-1 promoters. Further studies using chromatin immunoprecipitation assays demonstrated that E2F-1 binding to the apaf-1 and cyclinB promoters was increased and decreased, respectively, in CAPE-treated cells. Furthermore, E2F-1 silencing abolished CAPE-mediated effects on cell-cycle arrest, apoptosis and related gene expression. Taken together, these results indicate a crucial role for E2F-1 in CAPE-mediated cellular activities in cervical cancer cells.
Relation:	Febs Journal, v.280 n.11 pp.2581-2593
Appears in Collections:	[Dept. of Recreation and Health-Care Management] Periodical Articles

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