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Rapamycin-Induced Feedback Activation of mRNA Translation in Pancreatic Cancer

ABSTRACT: Rapamycin-Induced Feedback Activation of mRNA Translation in Pancreatic Cancer

PROVIDER: PRJNA937159 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23563656_1.fastq.gz	Fastqsanger.gz
	SRR23563656_2.fastq.gz	Fastqsanger.gz
	SRR23563657_1.fastq.gz	Fastqsanger.gz
	SRR23563657_2.fastq.gz	Fastqsanger.gz
	SRR23563658_1.fastq.gz	Fastqsanger.gz

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Rapamycin-Induced Feedback Activation of mRNA Translation in Pancreatic Cancer

Project description:We report mTOR inhibitor Rapamycin's specific and genome-wide effect on mRNA translation. Using ribosome footprinting in pancreatic cancer cells that lack 4EBP1 expression we establish the effect of mTOR-S6-dependent mRNA translation, and identify translation programs activated following mTOR inhibition.

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Modulation of nonsense-mediated decay by rapamycin

Project description:Rapamycin is a naturally occurring macrolide whose target is at the core of nutrient and stress regulation in a wide range of species. Despite well-established roles as an inhibitor of cap-dependent mRNA translation, relatively little is known about its effects on other modes of RNA processing. Here, we characterize the landscape of rapamycin-induced post-transcriptional gene regulation. Transcriptome analysis of rapamycin-treated cells revealed genome-wide changes in alternative mRNA splicing and pronounced changes in NMD-sensitive isoforms. We demonstrate that despite well-documented attenuation of cap-dependent mRNA translation, rapamycin can augment NMD of certain transcripts. Rapamycin-treatment significantly reduces the levels of both endogenous and exogenous PTC-containing mRNA isoforms and its effects are dose-, UPF1- and 4EBP-dependent manner. The PTC-containing SRSF6 transcript exhibits a shorter half-life upon rapamycin-treatment as compared to the non-PTC isoform. Rapamycin-treatment also caused depletion of PTC-containing mRNA isoforms from polyribosomes, underscoring the functional relationship between translation and NMD. Enhanced NMD activity also correlates with an enrichment of the nuclear Cap Binding Complex (CBC) in rapamycin-treated cells. Our data demonstrate that rapamycin modulates global RNA homeostasis by NMD.

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Project description:Measurement of mRNA abundance from the following cells lines (red) versus universal mouse reference RNA (green). Wildtype v-Abl transformed pre-B cells were treated for 12 hours with 2.5 uM imatinib mesylate, 10ng/mL rapamycin or nothing. Compound Based Treatment: wildtype v-Abl transformed pre-B cells were treated with imatinib mesylate (IMA), rapamycin (RAP) or nothing (NONE)

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Imatinib/Rapamycin mRNA abundance

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Dynamic mRNA gene expression following a rapamycin treatment

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Project description:Dynamic mRNA gene expression from the wildtype YSBN6 during a rapamycin treatment (rapamycin-induced downshift). Rapamycin was added to yeast cells growing exponentially on glutamine as sole nitrogen source. A sample was taken at steady-state 10 minutes before , and then 3, 7, 10, 14, 24, 56 and 120 minutes after rapamycin treatment. Biological triplicate gene expression was measured for samples -10, 7 and 24 minutes after shift, for a total of 14 chips. Changes were generally evaluated relative to the steady-state point (-10 minutes). Biological variability can be assessed from the replicates time points. Other dynamic omics data are associated with this dataset. Consult the publication for more details.

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TORC1 signaling pathway inhibition by rapamycin and caffeine affect lifespan, global gene expression and cell proliferation of fission yeast

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