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Effect of depletion of C15ORF48/miR-147 on gene expression in primary colonocytes [colonocytes]

ABSTRACT: Effect of depletion of C15ORF48/miR-147 on gene expression in primary colonocytes [colonocytes]

PROVIDER: PRJNA1033339 | ENA |

REPOSITORIES: ENA

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Effect of depletion of C15ORF48/miR-147 on gene expression in primary colonocytes

Project description:Effect of depletion of C15ORF48/miR-147 on gene expression in primary colonocytes

| PRJNA1033337 | ENA

Effect of depletion of C15ORF48/miR-147 on gene expression in primary colonocytes [HCT116]

Project description:Effect of depletion of C15ORF48/miR-147 on gene expression in primary colonocytes [HCT116]

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Effect of depletion of C15ORF48/miR-147 on gene expression in primary colonocytes [HCT116]

Project description:Chronic inflammation is epidemiologically linked to the pathogenesis of gastrointestinal diseases, including inflammatory bowel disease (IBD) and colorectal cancer (CRC). However, our understanding of the molecular mechanisms controlling gut inflammation remains insufficient, hindering the development of targeted therapies for IBD and CRC. In this study, we uncovered C15ORF48/miR-147 as a novel negative regulator of gut inflammation, operating through the modulation of epithelial cell metabolism. C15ORF48/miR-147 encodes two molecular products, C15ORF48 protein and miR-147-3p microRNA, which are predominantly expressed in intestinal epithelium. C15ORF48/miR-147 ablation leads to gut dysbiosis and exacerbates chemically-induced colitis in mice. C15ORF48 and miR-147-3p work together to suppress colonocyte metabolism and inflammatory responses, and thus bridging mitochondrial metabolism and inflammation.

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Effect of depletion of C15ORF48/miR-147 on gene expression in primary colonocytes [colonocytes]

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Gene expression affected by miR-147

Project description:The epithelial-mesenchymal transition (EMT) is a key developmental program that is often activated during cancer progression and may promote resistance to therapy. An analysis of patients (n = 71) profiled with both gene expression and a global microRNA assessment (~ 415 miRs) identified miR-147 as highly anti-correlated with an EMT gene expression signature score and postulated to reverse EMT (MET).We have found that miR-147 induced cancer cells to undergo MET phenotypically. It's necessary to investigate the genes affected by miR-147 to understand the mechanism. RNA extracted from miR-147 and non-coding miR transiently transfected HCT116 cells; gene expression then assayed using the Affymetrix GeneChip U133 Plus2.0 platform.

2014-11-01 | E-GEOD-51875 | biostudies-arrayexpress

Gene expression affected by miR-147

2014-11-01 | GSE51875 | GEO

Effect of depletion of C15ORF48/miR-147 on gene expression in primary colonocytes

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-07-17 | GSE246494 | GEO

Bacillus thuringiensis strain:147 | isolate:147

Project description:Bacillus thuringiensis strain:147 | isolate:147 Genome sequencing and assembly

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Effect of miR17-92 and miR-106b-25 loss in primary calvarial cells

Project description:Gene expression profiling of primary calvarial cells with miR-17-92:miR-106b-25 conditional deletion

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miR-638 promotes melanoma metastasis and protects melanoma cells from apoptosis and autophagy (mRNA)

Project description:MicroRNA (miRNA) expression profiling identified miR-638 as one of the most significantly overexpressed miRNAs in metastatic lesions compared with primary melanomas. miR-638 enhanced the tumourigenic properties of melanoma cells in vitro and lung colonization in vivo. mRNA expression profiling of miR-638 and antagomir-transduced cells identified new candidate genes as miR-638 targets, the majority of which is involved in p53-mediated apoptosis regulation. miR-638 depletion stimulated expression of p53 and its downstream target genes and induced apoptosis and autophagy in melanoma cells. miR-638 promoter analysis revealed transcription factor associated protein 2-? (TFAP2A) as a direct negative regulator of miR-638. Further analyses provided strong evidence for a double negative regulatory feedback loop between miR-638 and TFAP2A. Taken together, miR-638 may support melanoma progression by suppressing p53-mediated apoptosis pathways and by targeting the transcriptional repressor TFAP2A. Whole genome cDNA microarray (Illumina Human HT-12 v4 Expression BeadChip Kit, San Diego, CA 92122 USA) analyses were performed in duplicates using RNA extracted from SK-Mel-147 cells transfected with a non-targeting control, miR-638 or antagomiR-638.

2014-01-30 | E-GEOD-54493 | biostudies-arrayexpress

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