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

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

PROVIDER: PRJNA1033338 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26557456_1.fastq.gz	Fastqsanger.gz
	SRR26557456_2.fastq.gz	Fastqsanger.gz
	SRR26557457_1.fastq.gz	Fastqsanger.gz
	SRR26557457_2.fastq.gz	Fastqsanger.gz
	SRR26557458_1.fastq.gz	Fastqsanger.gz

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

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

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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

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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.

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Gene expression affected by miR-147

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Effect of depletion of MIB1 in HCT116 cells

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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.

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RNA-seq of depletion Mina53 in HCT116 p53+/+ cells and HCT116 p53-/- cells

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Transcriptional changes associated with miR-6762-5p expression in HCT116 cells

Project description:Decipher the direct and indirect targets of human miR-6762-5p by doxycyclin-inducible expression in HCT116 cells

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