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MiR-204 down-regulation elicited perturbation of a gene target signature common to human cholangiocarcinoma and gastric cancer.

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE81948 | GEO | 2017/04/10

SECONDARY ACCESSION(S): PRJNA323482

REPOSITORIES: GEO

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Homo sapiens

Project description:miR-204 down-regulation elicited perturbation of a gene target signature common to human cholangiocarcinoma and gastric cancer.

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Expression profile of HCT116 cells transfected with miR-204-5p

Project description:We have employed whole genome microarray expression profiling as a discovery platform to screen potential target genes of miR-204-5p in colorectal cancer cell HCT116. HCT116 cells were seeded in 6-cm2 tissue culture plates and transfected with the miR-204-5p mimic or negative control (NC) using Lipofectamine 2000 (Invitrogen, USA). After propagation for 48 hours, total RNA was extracted using TRIzol reagent (Invitrogen, USA). Expression profiling was performed using an Agilent human whole genome oligo microarray chip (4M-CM-^W44K) (Agilent, USA) Expression profiling in HCT116 cells was measured at 48 hours after transfection with miR-204-5p or negative control. Experiments were performed using the two samples without repeat experiment.

2014-07-30 | E-GEOD-59897 | biostudies-arrayexpress

Overexpression of microRNA-375 in medullary thyroid carcinoma cells hinders cell proliferation and improves the vandetanib efficacy effect in vitro

Project description:The global microRNA (miRNA) profiling expression was assessed in a large series of both sporadic and hereditary forms of medullary thyroid carcinomas (MTC), and to evaluate the biological function of major found altered miRNAs. For this purpose we investigated miRNA differential expression in tumoral vs adjacent non tumoral tissues from 62 MTC patients, and showed a specific overexpression of miR-375, -129-3p, -376c, -335, -96, -10a, -7, -429 and an underexpression of miR-451 in tumoral tissues. Since miR-375 was the most up-regulated miRNA, we thus decided to identify its targets by combining a transcriptomic signature of cells transfected either with premiR- or antagomiR-375 and an in silico analysis joining TT-cells mRNA specific signature from Cancer Cell Line Encyclopedia GEO dataset and miRNA prediction algorithms. Using this restrictive approach, we focused on miR-375 target SEC23A and validated a decreased expression of SEC23A by Western blotting and by immunohistochemistry in tumoral vs non tumoral adjacent thyroid epithelium. Furthermore, we observed that overexpression of miR-375 was associated with decreased proliferation and increased vandetanib response in vitro. Overall, our results showed an overexpression of miR-375 in MTC in association with a decrease of miR-375-potential targets including SEC23A. Additionnally, we postulate thatmiR-375 overexpression should be evaluated in MTC patients treated with the tyrosine kinase inhibitor, vandetanib.

2016-05-22 | GSE67742 | GEO

Expression profile of HCT116 cells transfected with miR-204-5p

2014-07-30 | GSE59897 | GEO

Development of microRNA expression signatures for gastric cancer

Project description:To further investigate of microRNA expression profile of gastric cancer, we have employed whole microRNA gene chip as a discovery platform to identify gene differential expression between gastric cancer tissues with mormal gastric tissues.Expression of four microRNAs (miR-125b,miR-451,miR-192b,miR-200b) from this signature was quantified and verified in the same RNA samples by real-time PCR. A total of 4 consecutive patients with gastric cancer undergoing elective surgery were entered into this study. After obtaining informed consent from the patients and after receiving the approval of the ethics committee, the following tissue samples were collected: tumor (3 × 3 × 5 mm) and adjacent normal tissues (3 × 3 × 5 mm).

2011-01-15 | E-GEOD-26645 | biostudies-arrayexpress

MiR-204-5p may Regulate Oxidative Stress in Myopia and Myopia-Related Retinopathy

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.

2024-01-26 | GSE253960 | GEO

Exercise promotes peripheral glycolysis through miR-204 induction in skeletal muscle

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.

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A critical role of microRNAs in human pulmonary arterial hypertension. miR-204: a novel therapeutic target (gene expression)

Project description:Pulmonary arterial hypertension (PAH) is a vascular remodeling disease characterized by enhanced pulmonary artery smooth muscle cell (PASMC) proliferation and suppressed apoptosis. Downregulation of the BMPR2 gene along with activation of the transcription factor NFAT have been implicated in the maintenance of pro-proliferative and anti-apoptotic stages of cells. Since an increasing number of microRNAs have been implicated in the regulation of genes specifically important for cell proliferation and apoptosis, we hypothesized that microRNAs might be associated with these cellular features in the etiology of PAH. We demonstrate that downregulation of one such microRNA (miR-204) in human PAH-PASMC promotes the activation of an Src/STAT3/NFAT axis that increases PAH-PASMC proliferation and their resistance to apoptosis. Stimulation experiments using the pro-PAH factors (PDGF, endothelin-1 and angiotensin II) and time course analysis in experimental PAH show that STAT3 activation leads to miR-204 downregulation, thereby activating an Src-dependent positive feedback loop sustaining STAT3 and activating NFAT. More importantly, restoring miR-204 expression decreases proliferation and resistance to apoptosis in human and in an experimental PAH model. Taken together, our study uncovers a new STAT3-miR-204-Src/STAT3/NFAT axis that links the STAT3-dependent downregulation of BMPR2 with the NFAT-mediated pro-proliferative and anti-apoptotic phenotype observed in PAH. Our data point toward a novel potential strategy for treating patients with PAH. Comparative expression profiling of PAH versus healthy patients to evaluate the modulated genes in the disease. Following the demonstration of the downregulation of miR-204 in PAH we want to investigate the effect of the inhibition (using antagomir) of miR-204 expression in PASMC cells.

2010-12-16 | E-GEOD-21280 | biostudies-arrayexpress

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