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Homo sapiens

ABSTRACT: Investigation of regulatory mechanism of NDRG1 by non-coding RNA upon reoxygenation

PROVIDER: PRJNA291803 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2157510_1.fastq.gz	Fastqsanger.gz
	SRR2157510_2.fastq.gz	Fastqsanger.gz
	SRR2157504_1.fastq.gz	Fastqsanger.gz
	SRR2157504_2.fastq.gz	Fastqsanger.gz
	SRR2157505_1.fastq.gz	Fastqsanger.gz

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MicroRNA-769-3p down-regulated NDRG1 and enhanced apoptosis in MCF-7 during reoxygenation.

Project description:In this study, breast cancer MCF-7 cells were cultured under 0.5% oxygen for 24 h followed by 24 h of reoxygenation. Cells was harvested at 0, 1, 12, and 24 h during reoxygenation, and examined the miRNA profile by Nanostring nCounter. Forty-three miRNAs had dramatic changes as compared with 0 h upon reoxygenation, with 63% (n=27) of the miRNAs up-regulated upon reoxygenation. Among these miRNAs, miR-769-3p, which was down-regulated in MCF-7 upon reoxygenation, was chosen for further investigation. The hypothesis was that the down-regulation of NDRG1 upon reoxygenation was regulated by miRNAs. To examine wether miRNAs regulate NDRG1 under 0.5% O2 concentrations, the miRNA expression profiles of MCF-7 cells under reoxygenation were examined. Cells were harvested at 0 (hypoxia control), 1, 12, and 24 h upon reoxygenation. Each profile was done in triplicate. The genomic profile of miRNAs was measured using NanoString nCounterÂ® miRNA Expression Assays.

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MicroRNA-769-3p down-regulated NDRG1 and enhanced apoptosis in MCF-7 during reoxygenation.

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Project description:MicroRNA-769-3p down-regulated NDRG1 and enhanced apoptosis in MCF-7 during reoxygenation.

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Project description:Host cells harbor various intrinsic mechanisms to restrict viral infections as a first line of antiviral defense. Viruses have evolved various countermeasures against these antiviral mechanisms. Here we show that N-Myc Downstream-Reguated Gene 1 (NDRG1) limits productive HCV infection by inhibiting viral assembly. Interestingly, HCV infection down-regulates NDRG1 protein and mRNA expression. Loss of NDRG1 increases the size and number of lipid droplets, which are the sites of HCV assembly. HCV suppresses NDRG1 expression by up-regulating MYC, which directly inhibits the transcription of NDRG1. Up-regulation of MYC also leads to reduced expression of NDRG1-specific kinase SGK1, resulting in markedly diminished phosphorylation of NDRG1. Knockdown of MYC during HCV infection rescues NDRG1 expression and phosphorylation, suggesting that MYC regulates NDRG1 at both transcriptional and post-translational levels. Overall, our results suggest that NDRG1 restricts HCV assembly by limiting lipid droplet formation. HCV counteracts this intrinsic antiviral mechanism by down-regulating NDRG1 via a MYC-dependent mechanism.

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