Analysis of differentially expressed genes in HepG2 after transfection with miR-192,miR-204 and siHOTTIP
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE60912 | GEO | 2017/02/09
SECONDARY ACCESSION(S): PRJNA259798
REPOSITORIES: GEO
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Project description:Downregulation of miR-192-5p and miR-204-5p in nonclassic apparent mineralocorticoid excess
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Project description:The aim of this study is to discover genes regulated by miR-204. Differential gene expression in HEK-293 cells transfected with miR-204-mimic compared to HEK-293 cells transfected with control oligo (HEK-293 control) was analyzed using the Agilent Human Whole Genome 4x44K gene expression array (Agilent Technologies, Santa Clara, CA). HEK-293 cells were transfected with either miR-204 or a control, and gene expression was analyzed using the Agilent Human Whole Genome 4x44K array. A dye-swap was performed.
2012-03-30 | E-GEOD-28400 | biostudies-arrayexpress
Project description:Cell cycle arrest in response to DNA damage is an important anti-tumorigenic mechanism. microRNAs (miRNAs) were shown recently to play key regulatory roles in cell cycle progression. For example, miR-34a is induced in response to p53 activation and mediates G1 arrest by down-regulating multiple cell cycle-related transcripts. Here we show that genotoxic stress promotes the p53-dependent up-regulation of the homologous miRNAs, miR -192 and miR-215. Like miR-34a, activation of miR-192/215 induces cell cycle arrest suggesting that multiple microRNA families operate in the p53 network. Furthermore, we define a downstream gene expression signature for miR-192/215 expression that includes a number of transcripts that regulate G1 and G2 checkpoints. Of these transcripts, 18 transcripts are direct targets of miR-192/215 and the observed cell cycle arrest likely results from a cooperative effect among the modulations of these genes by the miRNAs. Our results demonstrating a role for miR-192/215 in cell proliferation combined with recent observations that these miRNAs are under-expressed in primary cancers support the idea that miR-192 and miR-215 function as tumor-suppressors. Description: Transfection of siRNA luc, miR-192 or miR-215 into HCT116 Dicerex5, compared to mock-transfected cells, with mRNA expression profiled at 10h and 24h post-transfection. Species: Human Tissue: HCT116 Dicerex5 cell line (tissue of origin = human colorectal carcinoma); this cell line is hypomorphic for Dicer gene function. Dye-swap: no Negative control: siRNA luc Replicates per each timepoint: no
2010-06-24 | E-GEOD-13105 | biostudies-arrayexpress
Project description:The aim of this study is to discover genes regulated by miR-204. Differential gene expression in HEK-293 cells transfected with miR-204-mimic compared to HEK-293 cells transfected with control oligo (HEK-293 control) was analyzed using the Agilent Human Whole Genome 4x44K gene expression array (Agilent Technologies, Santa Clara, CA).
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Project description:Mechanisms underlying exercise induced insulin sensitization are of interest as exercise is a clinically critical option as a lifestyle intervention for diabetic patients. Some of microRNAs (miRNAs), which can be secreted from skeletal muscle after exercise, regulate insulin sensitivity and are used for diagnostic marker for diabetic patients. MiR-204 is well-known for its involvement in development, cancer, and metabolism. However, it is still unknown whether miR-204 associates with exerciseinduced glycemic control. In preliminary data, we found that endurance exercise of mice increases miR-204 expression levels in skeletal muscle. In chronic exercise mice model, miR-204 expression levels were increased with glycolytic enzymes in skeletal muscle. When hypoxia induced hypoxia inducible factor 1 alpha (HIF1α), miR-204 expression levels were increased. HIF1α overexpression also increased miR-204 expression levels. To corroborate the causality between miR-204 and glycolysis, miR-204 mimic was introduced to myoblast cell line, C2C12 myoblast cell line. After exposure to miR-204 mimic, C2C12 cells could increase the glycolysis rate measured by extracellular acidification rate. miR-204 mimics also increased mRNA expression levels of glycolytic enzymes. In vivo intravenous miR-204 administration to mice also increased the glucose clearance rate after refeeding of mice. MiR-204 increased blood glucose surge on earlier point of refeeding but promoted the blood glucose lowering on later point of refeeding. Skeletal muscle glycolytic enzymes were increased in mRNA expression levels by miR-204 injection. This finding suggests the novel physiological role of miR-204 in skeletal muscle glycolysis where insulin action is limited.
2024-09-04 | GSE276372 | GEO
Project description:There is high need of novel diagnostic and prognostic tools for tumors of the digestive system, such as gastric cancer and cholangiocarcinoma. We employed Affymetrix profiling of 15 gastric tumor tissues and 5 normals to evaluate the levels of miR-204 target genes. We performed extensive in silico analysis to identify a minimal gene target signature which anti-correlated with the levels of miR-204 and validated all of the findings on publicly available databases. We employed transient transfection experiments, clonogenic assays and cell cycle profiling to evaluate the dependency of the target genes signature of miR-204 and the biological consequences of miR-204 perturbation. Then we validate the data obtained in a cohort of tumoral and normal gastric samples, tumoral and normal cholangiocarcinoma samples. to statistically strengthen the genes signature obtained we analyzed data available on gastric, colangiocarcinoma, esophageal and colon database
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Project description:LncRNA MIR194-2HG and derived miR-194 and miR-192 were transcriptionally induced by HNF4A. The oncogenic driver BTF3L4 is identified to be a common target gene of miR-194 and miR-192. Our finding highlights that MIR194-2HG inhibits GC progression through activating the expression miR-192 and miR-194 and repressing BTF3L4 expression.
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Project description:Introduction: The mechanisms underlying myopia and myopia-related retinopathy remain not fully understood. We proposed to examine the function and underlying mechanisms of miR-204-5p in myopia development. Methods: The miR-204-5p expression level was assessed in the vitreous humor (VH) of a cohort consisting of 11 patients with high myopia (HM) and 16 control patients undergoing retinal surgery. The functional implications of miR-204-5p in ARPE-19 cells were assessed, encompassing cell aggressiveness. Thioredoxin-interacting protein (TXNIP) was found as a possible target of miR-204-5p through mRNA sequencing, and its interaction with miR-204-5p was confirmed employing luciferase assay and western blotting. Furthermore, the miR-204-5p function in regulating oxidative stress was examined by measuring reactive oxygen species (ROS) accumulation. Results: miR-204-5p was found to be significantly reduced in the VH of HM patients. Overexpression of miR-204-5p suppressed cell proliferation, migration, invasion, and apoptosis in ARPE-19 cells. The bioinformatics analysis demonstrated that miR-204-5p can modulate the genes associated with pathways relevant to myopia, including glycosaminoglycan (GAG) degradation, lysosome, and TGF−beta signaling pathway. The direct targeting of miR-204-5p on TXNIP has been confirmed through validation, and its downregulation mediated the miR-204-5p impacts on ARPE-19 cells. Moreover, miR-204-5p overexpression significantly reduced ROS accumulation by targeting TXNIP. Conclusion: Our findings revealed the possible contribution of the miR-204-5p/TXNIP axis in myopia development by regulating oxidative stress, which may provide new targets and novel therapeutic strategies to combat this prevalent and debilitating condition.
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