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Regular exercise suppresses steatosis-associated liver cancer development by degrading E2F1 and c-Myc via circadian gene upregulation

ABSTRACT: Regular exercise suppresses steatosis-associated liver cancer development by degrading E2F1 and c-Myc via circadian gene upregulation

PROVIDER: PRJNA1142455 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30054407.fastq.gz	Fastqsanger.gz
	SRR30054408.fastq.gz	Fastqsanger.gz
	SRR30054409.fastq.gz	Fastqsanger.gz
	SRR30054410.fastq.gz	Fastqsanger.gz
	SRR30054411.fastq.gz	Fastqsanger.gz

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Regular exercise suppresses steatosis-associated liver cancer development by degrading E2F1 and c-Myc via circadian gene upregulation

Project description:Regular exercise is believed to suppress cancer progression. However, the precise molecular mechanisms by which exercise prevents cancer development remain unclear. In this study, using a steatosis-associated liver cancer mouse model, we found that regular exercise at a speed of 18 m/min for 20 min daily suppressed liver cancer development. To explore the underlying mechanisms, we examined the gene expression profiles in the livers of the exercise and non-exercise groups. We extracted RNA from non-tumor and tumor tissues from each mouse liver and performed bulk RNA-seq analysis. The expressions of circadian genes, such as Per1 and Cry2, were upregulated in the exercise group. We further found that the expression of a series of E2F1 and c-Myc target genes that directly affect the proliferation of cancer cells was downregulated in the exercised group. However, the expression of these genes was transcriptionally unchanged but degraded at the post-translational level by exercise. Cry2, which is regulated by the Skp1-Cul1-FBXL3 (SCFFBXL3) ubiquitin ligase complex by binding to FBXL3, can form a complex with E2F1 and c-Myc, which we think is the mechanism to degrade them. Our study revealed a previously unknown mechanism by which exercise prevents cancer development.

2024-09-03 | GSE273579 | GEO

E2F1 ChIP-Seq on mouse hepatocytes overexpressing E2F1

Project description:E2F transcription factors are known regulators of the cell cycle, proliferation, apoptosis and differentiation. We reveal an essential role for E2F1 in liver through the regulation of glycolysis and lipogenesis. E2F1 deficiency leads to a decreased in glycolysis and de novo synthesis of fatty acids in hepatocytes. ChIP-Seq was performed to determine direct tagets of E2F1 in hepatocytes. We highlight that E2F1 directly binds the promoters of genes implicated in metabolic process and notably key lipogenic genes to control these pathways.

2015-12-01 | GSE74006 | GEO

E2F1 mediates SOX17 Deficiency-Induced Pulmonary Hypertension [scRNA-seq]

Project description:SRY-Box Transcription Factor 17 (SOX17) enhancers variants and mutations are found in patients with pulmonary arterial hypertension (PAH). In human PAH pulmonary endothelial cells, there is a significant downregulation of SOX17 expression. We hypothesized that SOX17 deficiency contributes to the pathogenesis of PAH and found that mice with endothelial specific disruption (ecKO Sox17) developed spontaneous pulmonary hypertension (PH) and exacerbated hypoxia-induced PH. Loss of SOX17 in lung ECs induced endothelial dysfunctions including upregulation of cell cycle programming and paracrine effect, proliferative and anti-apoptotic phenotypes, impaired cellular junction and BMP signaling. E2F Transcription Factor 1 (E2F1) signaling was showed to mediate the SOX17 deficiency-induced EC dysfunction. Pharmacological inhibition of E2F1 in ecKO Sox17 mice attenuated PH and cell cycle programming. Our study demonstrated that endothelial SOX17 deficiency induces PH through E2F1 and targeting E2F1 signaling represents a promising approach in PAH patients.

2023-06-27 | GSE218398 | GEO

The Effects of Regular Post-Exercise Cold Water Immersion on DNA methylation in Muscle Following 10-weeks of Strength Training

Project description:In this study, the primary objective was to characterise the impact of regular post-exercise (20 strength training sessions across 10 weeks) cold-water immersion (CWI) on DNA methhylation. Secondary to this, the effect of regular post-exercise CWI on strength gains and post-exercise soreness was investigated. We used microarrays to detail the global effects of CWI on DNA methylation in vastus lateralis muscle tissue.

2016-08-16 | GSE85621 | GEO

The Effects of Regular Post-Exercise Cold Water Immersion on Gene Expression in Muscle Following 10-weeks of Strength Training

Project description:In this study, the primary objective was to characterise the impact of regular post-exercise (20 strength training sessions across 10 weeks) cold-water immersion (CWI) on mRNA expression. Secondary to this, the effect of regular post-exercise CWI on strength gains and post-exercise soreness was investigated. We used microarrays to detail the global effects of CWI on gene expression in vastus lateralis muscle tissue.

2016-08-16 | GSE85620 | GEO

Expression data from U2OS ER-E2F1 cells after FOXO knockdown and E2F1 activation

Project description:Effect of FOXO knockdown on E2F1-mediated transcription

2012-07-06 | GSE39136 | GEO

Regular physical activity followed by detraining increases the sensitivity of global gene expression to acute exercise stress

Project description:To determine the influence of a previous physcial activity period (e.g., exercise) on global gene expression, we compared differential expression in sedentary (SED) and detrained (DETR) rats relative to trained (TR) rats with regular access to physcial activity.

2016-04-05 | GSE79894 | GEO

Non-steroidal Anti-inflammatory Drugs Decrease E2F1 Expression and Inhibit Cell Growth in Ovarian Cancer Cells

Project description:Epidemiological studies have shown that the regular use of non-steroidal anti-inflammatory (NSAIDs) drugs is associated with a reduced risk of various cancers. In addition, in vitro and experiments in mouse models have demonstrated that NSAIDs decrease tumor initiation and/or progression of several cancers. However, there are limited preclinical studies investigating the effects of NSAIDs in ovarian cancer. Here, we have studied the effects of two NSAIDs, diclofenac and indomethacin, in ovarian cancer cell lines and in a xenograft mouse model. Diclofenac and indomethacin treatment decreased cell growth by inducing cell cycle arrest and apoptosis. In addition, diclofenac and indomethacin reduced tumor volume in a xenograft model of ovarian cancer. To identify possible molecular pathways mediating the effects of NSAID treatment in ovarian cancer, we performed microarray analysis of ovarian cancer cells treated with indomethacin or diclofenac. Interestingly, several of the genes found downregulated following diclofenac or indomethacin treatment are transcriptional target genes of E2F1. E2F1 was downregulated at the mRNA and protein level upon treatment with diclofenac and indomethacin, and overexpression of E2F1 rescued cells from the growth inhibitory effects of diclofenac and indomethacin. In conclusion, NSAIDs diclofenac and indomethacin exert an anti-proliferative effect in ovarian cancer in vitro and in vivo and the effects of NSAIDs may be mediated, in part, by downregulation of E2F1.

2014-06-20 | GSE45052 | GEO

Expression level is a key determinant of E2F1-mediated cell fate

Project description:Purpose: dose response analysis of E2F1 target genes expression in flow-sorted fractions with increasing amounts of fluorescently labled E2F1 Methods:U2OS pTRIPZ-YFP-ER-E2F1 cells were grown in full serum-containing growth medium and treated with 500 ng/ml doxycycline for 48 hours followed by addition of 90 nM OHT for an additional 20 hours. Cells from different YFP fractions were sorted by flow cytometry. mRNA profiles were generated by deep sequencing using Illumina HiSeq 4000. Results: different target genes have different E2F1 activation thresholds. Numerous proliferation-related target genes are induced already by the lowest E2F1-levels. Intermediate E2F1 levels induce cdk inhibitors, which might be responsible for cell cycle arrest. Finally, although some apoptotic E2F1 targets are induced already by low E2F1 levels, many key apoptotic genes require higher E2F1 levels for induction. Conclusions: induction of different cell fates by increasing E2F1 levels might pertain to differential affinities of the targets.

2017-08-22 | GSE93365 | GEO

E2F1-regulated genes

Project description:Identification of E2F1-regulated genes that modulate the transition from quiescence into DNA synthesis, or have roles in apoptosis, signal transduction, membrane biology, and transcription repression. Keywords: other

2003-07-16 | GSE498 | GEO

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