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Transcriptional profiling of PC-3 human prostate cancer cells in response to caffeic acid phenethyl ester treatment

ABSTRACT: PC-3 prostate cancer cells were treated with caffeic acid phenethyl ester (CAPE) or vehicle control for 24 h and 72 h for transcription microarray analysis.

ORGANISM(S): Homo sapiens

SUBMITTER: Shih Sheng Jiang

PROVIDER: E-MTAB-773 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression profiling of caffeic acid phenethyl ester -treated human umbilical vein endothelial cells

Project description:This SuperSeries is composed of the following subset Series: GSE10413: Gene expression profiling of caffeic acid phenethyl ester-treated human umbilical vein endothelial cells-1 GSE10429: Gene expression profiling of caffeic acid phenethyl ester -treated human umbilical vein endothelial cells-2 Keywords: SuperSeries Refer to individual Series

2010-05-26 | E-GEOD-10465 | biostudies-arrayexpress

Gene expression profiling of caffeic acid phenethyl ester-treated human umbilical vein endothelial cells-2

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 Âµg/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.

2010-05-26 | E-GEOD-10429 | biostudies-arrayexpress

Gene expression profiling of caffeic acid phenethyl ester-treated human umbilical vein endothelial cells-1

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 Âµg/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.

2010-05-26 | E-GEOD-10413 | biostudies-arrayexpress

Protection of SH-SY5Y cells against 6-OHDA by 3,4-dihydroxybenzalacetone (DBL) and caffeic acid phenethyl ester (CAPE)

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.

2020-01-31 | GSE93639 | GEO

Gene expression profiling of caffeic acid phenethyl ester-treated human umbilical vein endothelial cells-1

2008-02-12 | GSE10413 | GEO

Gene expression profiling of caffeic acid phenethyl ester-treated human umbilical vein endothelial cells-2

2008-02-12 | GSE10429 | GEO

Expression data from Nasopharyngeal carcinoma (NPC) cell lines treated or untreated with Caffeic acid phenethyl ester (CAPE)

Project description:Expression data from Nasopharyngeal carcinoma (NPC) cell lines treated or untreated with Caffeic acid phenethyl ester (CAPE)

| PRJNA522690 | ENA

A chemical screen in zebrafish embryonic cells establishes that Akt activation is required for neural crest development [RNA-seq]

Project description:The neural crest is a dynamic progenitor cell population that arises at the border of neural and non-neural ectoderm. The inductive roles of FGF, Wnt, and BMP at the neural plate border are well established, but the signals required for subsequent neural crest development remain poorly characterized. Here, we conducted a screen in primary zebrafish embryo cultures for chemicals that decrease neural crest formation, as read out by crestin:EGFP expression. We found that the natural product caffeic acid phenethyl ester (CAPE) disrupts neural crest gene expression, migration, and melanocytic differentiation by reducing Sox10 activity. CAPE inhibits PI3K/Akt signaling specifically in FGF-stimulated cells, and neural crest defects in CAPE-treated embryos are suppressed by constitutively active Akt1. Inhibition of Akt activity by constitutively active PTEN similarly decreases crestin expression and Sox10 activity. Our study has identified Akt as a novel intracellular pathway required for neural crest development.

2017-08-17 | GSE95814 | GEO

A chemical screen in zebrafish embryonic cells establishes that Akt activation is required for neural crest development [ATAC-seq]

2017-08-17 | GSE95813 | GEO

Blocking Toxin function and Modulating Gut Microbiota: Caffeic Acid and its Derivatives as Potential Treatments for Clostridioides difficile Infections

Project description:<p>Clostridioides difficile infection (CDI) is the leading cause of hospital-acquired diarrhea that seriously threaten public health. Disruption of normal gut microbiota by the use of broad-spectrum antimicrobial agents enables C. difficile to proliferate in the colon. The emergence and prevalence of hypervirulent C. difficile strains result in increased morbidity, mortality and recurrence rates of CDI, thus creating a pressing need for novel therapeutics. The multi-domain toxins TcdA and TcdB are the primary determinant of CDI pathogenesis, renders them ideal drug targets in the anti-virulence paradigm. In this study, we identified caffeic acid and its derivatives as active inhibitors of TcdB via a cell-based high-throughput phenotypic screening. Further mechanistic investigations revealed that caffeic acid phenethyl ester (CAPE) could directly bind to TcdB, thus suppressing InsP6-induced autoproteolysis and inhibiting the glucosyltransferase activity. CAPE-treatment remarkably reduces the pathology of CDI in a murine infection model in terms of alleviated diarrhea symptom, decreased bacterial colonization and relieved histopathological lesions. Moreover, CAPE-treatment of C. difficile-challenged mice induces remarkable increase in the diversity and composition of the gut microbiota (e.g. Bacteroides) and alterations of gut metabolites (e.g. adenosine, D-proline and melatonin), which might partially contribute to the therapeutic outcomes of CAPE against CDI. Our results reveal the potential of CAPE as a therapeutic for the management of CDI, or CAPE might be served as a lead compound for the development of anti-virulence drug targeting TcdB.</p>

2024-06-04 | MTBLS9938 | MetaboLights

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