Ontology highlight
ABSTRACT:
PROVIDER: PRJNA868420 | ENA |
REPOSITORIES: ENA
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Project description:Quercetin is a flavonol modifying numerous cell processes with potent antiproliferative effects on cancer cell-lines. The aim of this study was to explore by gene-array analysis the effect of quercetin on cancer-related gene expression in HepG2 cells, followed by verification with RT-PCR and analysis of the expected phenotypic changes (migration, cell cycle, cell proliferation). Quercetin induces significant changes on cell-adhesion related genes, leading to reduced migratory capacity and disorganization of the actin cytoskeleton. Several genes related to DNA functions, cellular metabolism and signal-transducer activities were also modified, while an early effect on G–protein related cascades possibly via protease-activated receptor 2 and phospholipase C-γ1 was identified. Cyclin-D associated events in G1 and ubiquitin-dependent degradation of cyclin-D1 were also affected, resulting in cell-cycle arrest without activation of apoptosis pathways. In conclusion quercetin (3μM) exerts its cellular effects by modifying numerous genes related to mechanisms involved in cancer initiation and promotion.
2009-03-11 | GSE15162 | GEO
Project description:Quercetin is a flavonol modifying numerous cell processes with potent antiproliferative effects on cancer cell-lines. The aim of this study was to explore by gene-array analysis the effect of quercetin on cancer-related gene expression in HepG2 cells, followed by verification with RT-PCR and analysis of the expected phenotypic changes (migration, cell cycle, cell proliferation). Quercetin induces significant changes on cell-adhesion related genes, leading to reduced migratory capacity and disorganization of the actin cytoskeleton. Several genes related to DNA functions, cellular metabolism and signal-transducer activities were also modified, while an early effect on G–protein related cascades possibly via protease-activated receptor 2 and phospholipase C-?1 was identified. Cyclin-D associated events in G1 and ubiquitin-dependent degradation of cyclin-D1 were also affected, resulting in cell-cycle arrest without activation of apoptosis pathways. In conclusion quercetin (3?M) exerts its cellular effects by modifying numerous genes related to mechanisms involved in cancer initiation and promotion. HepG2 cells were serum starved for 24 hours and were then treated with serum free medium with or without quercetin (3?M). Total RNA was collected at 2, 4, 12 and 24 hours and was used for gene-array experiments.
2009-03-11 | E-GEOD-15162 | biostudies-arrayexpress
Project description:Quercetin has been shown to act as an anti-carcinogen in experimental colorectal cancer (CRC). The aim of the present study was to characterise transcriptome and proteome changes occurring in the distal colon mucosa of rats supplemented with 10 g quercetin/kg diet for 11 weeks. Transcriptome data analysed with Gene Set Enrichment Analysis showed that quercetin significantly downregulated the potentially oncogenic mitogen-activated protein kinase (Mapk) pathway. In addition, quercetin enhanced expression of tumor suppressor genes, including Pten, Tp53 and Msh2, and of cell cycle inhibitors, including Mutyh. Furthermore, dietary quercetin enhanced genes involved in phase I and II metabolism, including Fmo5, Ephx1, Ephx2 and Gpx2. Quercetin increased PPARα target genes, and concomitantly enhanced expression genes in volved in of mitochondrial fatty acid degradation. Proteomics performed in the same samples revealed 33 affected proteins, of which 4 glycolysis enzymes and 3 heatshock proteins were decreased. A proteome-transcriptome comparison showed a low correlation, but both pointed out towards altered energy metabolism. In conclusion, transcriptomics combined with proteomics showed that dietary quercetin evoked changes contrary to those found in colorectal carcinogenesis. These tumor-protective mechanisms were associated with a shift in energy production pathways, pointing at decreased glycolysis in the cytoplasm towards increased fatty acid degradation in the mitochondria. Experiment Overall Design: After an 11-week diet, rats fed quercetin or the control diet were sacrificed and fold changes in gene expression were detemined as quercetin (n=4) vs. control (n=4)
2008-06-15 | E-GEOD-7479 | biostudies-arrayexpress
Project description:Quercetin has been shown to act as an anti-carcinogen in experimental colorectal cancer (CRC). The aim of the present study was to characterise transcriptome and proteome changes occurring in the distal colon mucosa of rats supplemented with 10 g quercetin/kg diet for 11 weeks. Transcriptome data analysed with Gene Set Enrichment Analysis showed that quercetin significantly downregulated the potentially oncogenic mitogen-activated protein kinase (Mapk) pathway. In addition, quercetin enhanced expression of tumor suppressor genes, including Pten, Tp53 and Msh2, and of cell cycle inhibitors, including Mutyh. Furthermore, dietary quercetin enhanced genes involved in phase I and II metabolism, including Fmo5, Ephx1, Ephx2 and Gpx2. Quercetin increased PPARα target genes, and concomitantly enhanced expression genes in volved in of mitochondrial fatty acid degradation. Proteomics performed in the same samples revealed 33 affected proteins, of which 4 glycolysis enzymes and 3 heatshock proteins were decreased. A proteome-transcriptome comparison showed a low correlation, but both pointed out towards altered energy metabolism. In conclusion, transcriptomics combined with proteomics showed that dietary quercetin evoked changes contrary to those found in colorectal carcinogenesis. These tumor-protective mechanisms were associated with a shift in energy production pathways, pointing at decreased glycolysis in the cytoplasm towards increased fatty acid degradation in the mitochondria. Keywords: Transscriptomics, proteomics, quercetin-exposed and control rats
2008-01-01 | GSE7479 | GEO
Project description:To determine the effect of consumption of a quercetin-rich diet on obesity and dysregulated hepatic gene expression, C56BL/6J mice were fed for 20 weeks on control or a Western diet high in fat, cholesterol and sucrose, both with or without 0.05% quercetin. Chronic dietary intake of quercetin reduced body weight gain and visceral and liver fat accumulation, and improved hyperglyceamia, hyperinsulinaemia, dyslipidaemia in mice fed a Western-style diet. Feeding a Western-style diet altered expression of genes related to inflammatory responses, lipid metabolism and oxidative phosphorylation in C57BL/6J mice after 20 weeks. The results from exhaustive gene expression analysis showed that quercetin minimally influenced hepatic gene expression in mice fed the Western diet. The gene screening results (GSEA) were consistent with the notion that it did improve mitochondrial function to some extent. Quantitative RT-PCR analysis indicated that quercetin did influence important regulators of fat accumulation and metabolic disorders. Our results suggest that quercetin reduces fat accumulation presumably through decreasing oxidative stress and increasing PPARα expression, and the following improvement of gene expression related to steatosis in the liver.
2012-05-30 | GSE38141 | GEO