Project description:Small-cell lung cancer H446 cells were treated with CAPE. The regulation mediated by miR-3960 after CAPE treatment was explored and the altered signaling pathways were predicted in a bioinformatics analysis.CAPE decreased the expression of yes-associated protein 1 (YAP1) and cellular myelocytomatosis oncogene (c-MYC) protein. Moreover, the upregulation of miR-3960 by CAPE contributed to CAPE-induced apoptosis. The knockdown of miR-3960 decreased the CAPE-induced apoptosis.
Project description:Caffeic acid phenethyl ester (CAPE), derived from various plant sources, has been shown to ameliorate ischemia/reperfusion (I/R) injury in vivo, and this has been attributed to its ability to reduce the oxidative stress. Here we investigated the cytoprotection of CAPE against menadione (MD)-induced oxidative stress in human umbilical vein endothelial cells (HUVEC) to evaluate potential gene expression involvement. CAPE exhibited dose-dependent cytoprotection of HUVEC that required preincubation. A gene screen with microarrays was performed to identify the potential cytoprotective gene(s) induced by CAPE. Heme oxygenase-1 (HO-1) was highly upregulated by CAPE and this was confirmed with reverse transcriptase polymerase chain reaction (RT-PCR) and western blotting. Keywords: Gene expression in HUVEC, CAPE cytoprotective dose response
Project description:Caffeic acid phenethyl ester (CAPE), derived from various plant sources, has been shown to ameliorate ischemia/reperfusion (I/R) injury in vivo, and this has been attributed to its ability to reduce the oxidative stress. Here we investigated the cytoprotection of CAPE against menadione (MD)-induced oxidative stress in human umbilical vein endothelial cells (HUVEC) to evaluate potential gene expression involvement. CAPE exhibited dose-dependent cytoprotection of HUVEC that required preincubation. A gene screen with microarrays was performed to identify the potential cytoprotective gene(s) induced by CAPE. Heme oxygenase-1 (HO-1) was highly upregulated by CAPE and this was confirmed with reverse transcriptase polymerase chain reaction (RT-PCR) and western blotting. Keywords: gene expression in HUVEC, CAPE cytoprotective dose response
Project description:CAPE has anti-bacterial and viral infection, anti-oxidant, anti-inflammatory, and anti-tumor properties.We found that CAPE suppressed the proliferation and colony-formation ability of NPC cells. We used microarrays to identify differential genes regulated by CAPE in NPC cells and futher analys the potential GO and pathway
Project description:Caffeic acid phenethyl ester (CAPE), derived from various plant sources, has been shown to ameliorate ischemia/reperfusion (I/R) injury in vivo, and this has been attributed to its ability to reduce the oxidative stress. Here we investigated the cytoprotection of CAPE against menadione (MD)-induced oxidative stress in human umbilical vein endothelial cells (HUVEC) to evaluate potential gene expression involvement. CAPE exhibited dose-dependent cytoprotection of HUVEC that required preincubation. A gene screen with microarrays was performed to identify the potential cytoprotective gene(s) induced by CAPE. Heme oxygenase-1 (HO-1) was highly upregulated by CAPE and this was confirmed with reverse transcriptase polymerase chain reaction (RT-PCR) and western blotting. Keywords: gene expression in HUVEC, CAPE cytoprotective dose response Confluent HUVEC were incubated with cytoprotective dose of CAPE at 5 µg/ml or 0.1% DMSO as vehicle control for 6 hrs. Both treatments were done in triplicates. Total RNA was isolated at the end of the treatment and applied to microarray experiments in order to identify transcriptional response of HUVEC to CAPE. Microarray experiments were based on a two-color reference design using human universal reference RNA to compare results bwtween CAPE treatment and vehicle control groups.
Project description:Caffeic acid phenethyl ester (CAPE), derived from various plant sources, has been shown to ameliorate ischemia/reperfusion (I/R) injury in vivo, and this has been attributed to its ability to reduce the oxidative stress. Here we investigated the cytoprotection of CAPE against menadione (MD)-induced oxidative stress in human umbilical vein endothelial cells (HUVEC) to evaluate potential gene expression involvement. CAPE exhibited dose-dependent cytoprotection of HUVEC that required preincubation. A gene screen with microarrays was performed to identify the potential cytoprotective gene(s) induced by CAPE. Heme oxygenase-1 (HO-1) was highly upregulated by CAPE and this was confirmed with reverse transcriptase polymerase chain reaction (RT-PCR) and western blotting. Keywords: Gene expression in HUVEC, CAPE cytoprotective dose response Confluent HUVEC were incubated with cytoprotective dose of CAPE at 5 µg/ml or 0.1% DMSO as vehicle control for 6 hrs. Both treatments were done in triplicates. Total RNA was isolated at the end of the treatment and applied to microarray experiments in order to identify transcriptional response of HUVEC to CAPE. Microarray experiments were based on a two-color reference design using human universal reference RNA to compare results bwtween CAPE treatment and vehicle control groups.
Project description:3,4-dihydroxybenzalacetone (DBL) and Caffeic acid phenethyl ester (CAPE) are both catechol-containing phenylpropanoid derivatives. In the present study, we compared the neuroprotective characteristics of these compounds and other phenylpropanoid derivatives against Parkinson’s disease-related neurotoxin 6-hydroxydopamine (6-OHDA). Pretreatment of human SH-SY5Y neuroblastoma cells with DBL or CAPE, but not with other compounds, prevented 6-OHDA-induced cell death, with marked effects observed for CAPE. To identify the mechanism, we compared gene expression profiles induced by these compounds in SH-SY5Y cells.
