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Inhibitory mechanism of combined hydroxychavicol with epigallocatechin-3-gallate against glioma cancer cell lines: A transcriptomic analysis

ABSTRACT: Inhibitory mechanism of combined hydroxychavicol with epigallocatechin-3-gallate against glioma cancer cell lines: A transcriptomic analysis

PROVIDER: PRJNA798066 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17646507.fastq.gz	Fastqsanger.gz
	SRR17646507_1.fastq.gz	Fastqsanger.gz
	SRR17646507_2.fastq.gz	Fastqsanger.gz
	SRR17646508.fastq.gz	Fastqsanger.gz
	SRR17646508_1.fastq.gz	Fastqsanger.gz

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Inhibitory mechanism of combined hydroxychavicol with epigallocatechin-3-gallate against glioma cancer cell lines: A transcriptomic analysis

Project description:We reported the molecular mechanisms of low combination doses of epigallocatechin-3-gallate and hydroxychavicol (EGCG+HC) in glioma cell lines 1321N1 and LN18. Using high throughput RNA sequencing, combined EGCG+HC exerted its anticancer effect by downregulating the axon guidance process and metabolic pathways, while simultaneously interfering with endoplasmic reticulum unfolded protein response pathway. Furthermore, EGCG+HC exerted its apoptotic effect through the alteration of mitochondrial genes such as MT-CO3 and MT-RNR2 in 1321N1 and LN18 cells respectively. EGCG+HC dynamically altered DYNLL1 alternative splicing expression in 1321N1 and DLD splicing expression in LN18 cell lines.

2022-04-13 | GSE193838 | GEO

Epigallocatechin Gallate modulates microglia phenotype

Project description:Epigallocatechin Gallate modulates microglia phenotype

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Epigallocatechin Gallate modulates microglia phenotype

Project description:We have identified Epigallocatechin Gallate (EGCG) as a potent modulator of microglia function. Our aim was to determine whether EGCG affects the transcriptome of microglia and identify genes and gene sets that may underly the effects of EGCG on microglia function.

2024-07-17 | GSE208144 | GEO

TLR 4 Signaling Inhibitory Pathway Induced by Green Tea Polyphenol Epigallocatechin-3-Gallate through 67-kDa Laminin Receptor

Project description:Epigallocatechin-3-gallate (EGCG), a major active polyphenol of green tea, has been shown to downregulate inflammatory responses in macrophages; however, the underlying mechanism has not been understood. Recently, we identified the 67-kDa laminin receptor (67LR) as a cell-surface EGCG receptor that mediates the anti-cancer action of EGCG at physiologically relevant concentrations (0.1-1 mM). Here we show the molecular basis for the downregulation of TLR4 signal transduction by EGCG at 1 mM in macrophages. Anti-67LR antibody treatment or RNAi-mediated silencing of 67LR resulted in abrogation of the inhibitory action of EGCG on LPS-induced activation of downstream signaling pathways and target gene expressions. Additionally, we found that EGCG reduced the TLR4 expression through 67LR. Interestingly, EGCG induced a rapid upregulation of Tollip protein, a negative regulator of TLR-signaling, and this EGCG action was prevented by 67LR silencing or anti-67LR antibody treatment. RNAi-mediated silencing of Tollip impaired the TLR4 signaling inhibitory activity of EGCG. Taken together, these findings demonstrate that 67LR plays a critical role in mediating anti-inflammatory action of a physiologically relevant EGCG and Tollip expression could be modulated through 67LR. These results provide a new insight into the understanding of negative regulatory mechanisms for TLR4 signaling pathway and consequent inflammatory responses which are implicated in the development and progression of many chronic diseases. We quantified expression profile of 210 inflammatory-relating genes in the 67LR-downregulated cells treated with LPS or/and EGCG by microarray

2010-04-20 | E-GEOD-21320 | biostudies-arrayexpress

Global gene profiling of (-)-Epigallocatechin-3-gallate (EGCG)-induced neuronal death

Project description:Alzheimer’s disease (AD) is the most common form of adult-onset dementia with severe intellectual deterioration and is characterised by the accumulation of the amyloid-β (Aβ) peptides and the presence of hyperphosphorylated microtubule- associated protein, tau. (-)-Epigallocatechin-3-gallate (EGCG) – a polyphenolic catechin found in green tea leaves, not only acts as a proteasome inhibitor, it is also involved in neuroprotection.

2013-12-31 | GSE22996 | GEO

Global gene profiling of (-)-Epigallocatechin-3-gallate (EGCG)-induced neuronal death

2013-12-31 | E-GEOD-22996 | biostudies-arrayexpress

TLR 4 Signaling Inhibitory Pathway Induced by Green Tea Polyphenol Epigallocatechin-3-Gallate through 67-kDa Laminin Receptor

2010-04-20 | GSE21320 | GEO

microRNA profiling of HepG2 cells: control vs treatment with cacao, grape seed proanthocyanidin extract or epigallocatechin gallate

Project description:Mi(cro)RNAs are small non-coding RNAs of 18-25 nucleotides in length that modulate gene expression at the post-transcriptional level. These RNAs have been shown to be involved in a several biological processes, human diseases and metabolic disorders. Proanthocyanidins, which are the most abundant polyphenol class in the human diet, have positive heath effects on a variety of metabolic disorders such as inflammation, obesity, diabetes and insulin resistance. The present study aimed to evaluate whether proanthocyanidin-rich natural extracts modulate miRNA expression. Using microarray analysis and Q-PCR, we investigated miRNA expression in HepG2 cells treated with proanthocyanidins. Our results showed that when HepG2 cells were treated with grape seed proanthocyanidin extract (GSPE), cocoa proanthocyanidin extract (CPE) or pure epigallocatechin gallate isolated from green tea (EGCG), fifteen, six and five differentially expressed miRNAs, respectively, were identified out of 904 mRNAs. Specifically, miR-30b* was downregulated by the three treatments, and treatment with GSPE or CPE upregulated miR-1224-3p, miR-197 and miR-532-3p. Therefore, these results provide evidence of the capacity of dietary proanthocyanidins to influence microRNA expression, revealing a new mechanism of action of proanthocyanidins. microRNA profiling of Human hepatocellular liver carcinoma cell line (HepG2) comparing control untreated HepG2 cells with cells treated with grape seed proanthocyanidin extract (100 mg/L, 5h), cacao proanthocyanidin extract (100 mg/L, 5h) or epigallocatechin gallate (50 mg/L, 5h). Two biologival replicates were used for control and treated cells with one replicate per array.

2014-07-01 | E-GEOD-30575 | biostudies-arrayexpress

Epigallocatechin gallate delays age-related cataract development via the RASSF2/AKT pathway

Project description:Epigallocatechin gallate delays age-related cataract development via the RASSF2/AKT pathway

| PRJNA875091 | ENA

Epigallocatechin-3-gallate restores hippocampal proteomic alterations driven by Dyrk1A overexpression in mice

Project description:The inhibition of DYRK1A (Dual Specificity Tyrosine-Phosphorylation-Regulated Kinase 1A) activity, triplicated in trisomy 21 subjects, has been proved as a promising therapy for Down syndrome. Epigallocatechin-3-gallate (EGCG), a polyphenol of green tea, is an allosteric inhibitor of DYRK1A that showed beneficial pro-cognitive effects in clinical trials with DS individuals. However, EGCG induces several pharmacological effects, and there is no proof that the observed improvements result from DYRK1A inhibition. Besides, the direct consequences of Dyrk1A overexpression are not well defined. We therefore used quantitative proteomics to decipher the proteome and phosphoproteome alterations resulting from Dyrk1A overexpression and its inhibition to get insight into the mechanism of action of EGCG. Towards this aim, we used mice overexpressing Dyrk1A, and compared the hippocampal proteome and phosphoproteome with their wild type counterparts, in basal conditions, and after treatment with EGCG. Moreover, given that the human clinical trials found that the effects of EGCG potentiated the effects of cognitive stimulation, we also included in our study treatment with environmental enrichment and its combination with EGCG. We found that DYRK1A overexpression leads to alterations in protein and phosphoprotein levels of hundreds of proteins, and that the levels of proteins involved in key postsynaptic pathways are restored by the cognitive enhancer treatments, which could help conceiving new therapeutic strategies.

2019-12-11 | PXD010689 | Pride

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