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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE30575 | GEO | 2014/07/01

SECONDARY ACCESSION(S): PRJNA144641

REPOSITORIES: GEO

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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

miR-625-3p regulates oxaliplatin resistance by targeting MAP2K6-p38 signaling in human colorectal adenocarcinoma cells

Project description:Oxaliplatin (oxPt) resistance in colorectal cancers (CRC) is a major unsolved problem. Consequently, predictive markers and a better understanding of resistance mechanisms are urgently needed. To investigate if the recently identified predictive miR-625-3p is functionally involved in oxPt resistance, stable and inducible models of miR-625-3p dysregulation were analyzed. Ectopic expression of miR-625-3p in CRC cells led to increased resistance towards oxPt. The mitogen-activated protein kinase (MAPK) kinase 6 (MAP2K6/MKK6) – an activator of p38 MAPK - was identified as a functional target of miR-625-3p, and, in agreement, was down-regulated in patients not responding to oxPt therapy. The miR-625-3p resistance phenotype could be reversed by anti-miR-625-3p treatment and by ectopic expression of a miR-625-3p insensitive MAP2K6 variant. Transcriptome, proteome and phosphoproteome profiles revealed inactivation of MAP2K6-p38 signaling as a possible driving force behind oxPt resistance. We conclude that miR-625-3p induces oxPt resistance by abrogating MAP2K6-p38 regulated apoptosis and cell cycle control networks.

2017-03-29 | MSV000080762 | MassIVE

RNAi knock down of miR-30a-3p in human HepG2 cells to identify the target transcripts against miR-30a-3p in vivo

Project description:Human miR-30a-3p was knocked-down in HepG2 using siRNA duplex against the miRNA precursor, and compared to control cells on GeneChip to identify the target transcripts against miR-30a-3p in vivo.

2006-01-01 | E-MEXP-456 | biostudies-arrayexpress

Long non-coding RNA HOTTIP promotes CCL3 expression and induces cartilage degradation by sponging miR-455-3p

Project description:Long non-coding RNAs (lncRNAs) play pivotal roles in diseases such as osteoarthritis (OA). However, knowledge of the biological roles of lncRNAs is limited in OA. We aimed to explore the biological function and molecular mechanism of HOTTIP in chondrogenesis and cartilage degradation. We used the human mesenchymal stem cell (MSC) model of chondrogenesis, in parallel with, tissue biopsies from normal and OA cartilage to detect HOTTIP, CCL3, and miR-455-3p expression in vitro. Biological interactions between HOTTIP and miR-455-3p were determined by RNA silencing and overexpression in vitro. We evaluated the effect of HOTTIP on chondrogenesis and degeneration, and its regulation of miR-455-3p via competing endogenous RNA (ceRNA). Our in vitro ceRNA findings were further confirmed within animal models in vivo. Mechanisms of ceRNAs were determined by bioinformatic analysis, a luciferase reporter system, RNA pull-down, and RNA immunoprecipitation (RIP) assays. We found reduced miR-455-3p expression and significantly upregulated lncRNA HOTTIP and CCL3 expression in OA cartilage tissues and chondrocytes. The expression of HOTTIP and CCL3 was increased in chondrocytes treated with interleukin-1β (IL-1β) in vitro. Knockdown of HOTTIP promoted cartilage-specific gene expression and suppressed CCL3. Conversely, HOTTIP overexpression reduced cartilage-specific genes and increased CCL3. Notably, HOTTIP negatively regulated miR-455-3p and increased CCL3 levels in human primary chondrocytes. Mechanistic investigations indicated that HOTTIP functioned as ceRNA for miR-455-3p enhanced CCL3 expression. Taken together, the ceRNA regulatory network of HOTTIP/miR-455-3p/CCL3 plays a critical role in OA pathogenesis and suggests HOTTIP is a potential target in OA therapy.

2019-08-12 | PXD014988 | Pride

miR-552-3p modulates transcriptional activities of FXR and LXR to meliorate hepatic glycolipid metabolism disorder

Project description:According to our previous discovery that miR-552-3p could regulate the gene expression both in cytoplasm and nucleus. Furthermore, we found the sequence in miR-552-3p was similar with cis-elements of NR1 subfamily, the important regulator of glycolipid metabolism, suggesting miR-552-3p may play a pivotal role in metabolism. To find the genes regulated by miR-5523-p, RNA-seq was used and the difference expression genes in HepG2 cells transfected with miR-552-3p or negative control was detected. Meanwhile, to found which genes are regulated by cytoplasmic miR-552-3p or nuclear miR-552-3p, importin8 expression was silenced by siRNA in the HepG2 cell and the effect of miR-552-3p on the genes expression was detected. The results of this study are showed the genes regulated by miR-552-3p and distinguish which genes are regulated by the cytoplasmic miR-552-3p or nuclear miR-552-3p.

2020-07-15 | GSE154384 | GEO

Grape Proanthocyanidins Modulate MicroRNA Expression in Human pancreatic cancer cells

Project description:Mi(cro)RNAs are small non-coding RNAs of 18-25 nucleotides in length that modulate gene expression at the posttranscriptional level. Grape seed proanthocyanidins (GSPs), a biologically active component of grape seeds, have been shown to have positive effects on anti-cancer. In current study, to explore whether GSPs can regulate miRNA expression and possible molecular mechanisms involved in anti-cancer, we prepared the pancreatic cancer (PC) cells samples (SS3, SS12 and SS24) at 3, 12 and 24h after GSPs treatments respectively; and control samples (SC3, SC12 and SC24) were also collected accordingly. miRNA-seq transcriptome comparisons were performed, and 26, 85 and 85 differentially expressed (DE) miRNA were identified among SS3 vs. SC3, SS12 vs. SC12 and SS24 vs. SC24 respectively, indicating the GSPs treatments could modulate the expression of miRNAs globally. Subsequently, 74, 598 and 1204 target genes of these DE miRNAs were predicted in three comparisons, and GO and KEGG analysis revealed that multiple target genes were associated with proliferation and apoptosis of PC cells. Moreover, interaction network analyis of DE miRNAs and target genes associated with PC were also carried out, and fabulous co-expression relationships further suggested that GSPs treatment could probably repress the proliferation of PC cells by modulating the miRNAs expression

2019-03-20 | GSE107409 | GEO

Guanidineacetic acid regulate myogenic differentiation through miR-133a-5 and miR-1a-3p co-mediated PI3K-Akt-mTOR signaling pathway

Project description:Through small RNA sequencing, we finded that a total of 8 miRNAs, including miR-133a-3p and miR-1a-3p cluster, showed differential expression after guanidineacetic acid supplement. To further study the function of miR-133a-3p and miR-1a-3p in guanidineacetic acid induce myotube hypertrophy, we transfected miR-133a-3p and miR-1a-3p mimics, that also induce myotube hypertrophy. Through bioinformatics and dual-luciferase reporter system, the target gene of miR-133a-3p and miR-1a-3p were respectively determined. Meanwhile, miR-133a-3p and miR-1a-3p modulate PI3K-Akt-mTOR signaling pathway by restraining target gene expression.

2019-05-17 | GSE118528 | GEO

miR-625-3p regulates oxaliplatin resistance by targeting MAP2K6-p38 signaling in human colorectal adenocarcinoma cells

2016-08-12 | PXD002172 | Pride

5b763f6e-2031-4d46-913d-ee7491e7e50c - samples

Project description:iPSC-derived neurons were treated with mimics and inhibitors of the miRNAs miR-150-5p, hsa-mir-193a-3p and hsa-miR-19b-3p. RNA-sequencing was then performed to examine the effects of miRNA up-regulation and inhibition.

| EGAD00001006844 | EGA

Effect of mmu-miR-193b-3p and miR-365a-3p ectopic expression on the transcriptome of mouse cutaneous Squamous Cell Carcinoma cells

Project description:The mouse mSCC-20 cell line was transfected with 5nM of mmu-pre-miR-193b-3p, pre-miR-365a-3p or pre-miR-NC1. Total RNAs were extracted 30 h after transfection and hybridized on microarrays. One color experiment with 3 experimental conditions : miR-NC1- (n=4), miR-193b-3p- (n=2) and miR-365-3p- (n=2) transfected cells, corresponding to a total of 8 samples.

2014-02-03 | E-GEOD-52381 | biostudies-arrayexpress

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