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Molecular mechanism impacted by circadian disruption underscores the importance of timed anti-cancer treatment

ABSTRACT: Molecular mechanism impacted by circadian disruption underscores the importance of timed anti-cancer treatment

PROVIDER: PRJNA489887 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7807530.fastq.gz	Fastqsanger.gz
	SRR7807540.fastq.gz	Fastqsanger.gz
	SRR7807550.fastq.gz	Fastqsanger.gz
	SRR7807560.fastq.gz	Fastqsanger.gz
	SRR7807570.fastq.gz	Fastqsanger.gz

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Molecular mechanism impacted by circadian disruption underscores the importance of timed anti-cancer treatment

Project description:Circadian disruption has multiple pathological consequences, but the underlying mechanisms are largely unclear. To address such mechanisms, we subjected cultured cells to chronic circadian desynchrony (CCD), mimicking a chronic jet-lag paradigm, and assayed a range of cellular functions. The results indicated a specific circadian clock-dependent increase in cell proliferation. Transcriptome analysis revealed upregulation of G1-S-phase transition genes (cMyc, CyclinD1/3, Cdt1), concomitant with increased phosphorylation of the Retinoblastoma protein (Rb) by Cyclin D kinase 4/6 (CDK4/6) and increased G1-S progression. Phospho-Rb (Ser807/811) was found to oscillate in a circadian fashion and exhibit phase-shifted rhythms in circadian desynchronized cells. A CDK4/6 inhibitor approved for cancer treatment reduced growth of cultured cells and mouse tumors in a time-of-day specific manner, but the time dependence was lost with CCD. Our study identifies a mechanism that underlies effects of circadian disruption on tumor growth and underscores the importance of treatment timed to endogenous circadian rhythms.

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Timed topical dexamethasone eye drops improve mitochondrial function to suppress severe retinopathy of prematurity.

Project description:Pathological neovascularization (NV) can cause visual impairment in retinopathy of prematurity (ROP). Current treatments addressing vasoproliferative (Phase II) ROP are costly and can lead to severe complications. We show that well-timed topical 0.1% dexamethasone eye drops during early retinal neovascular formation prevents NV in five extremely preterm infants at high risk for ROP and in mouse oxygen-induced retinopathy (OIR) modeling ROP. In OIR mice, daily treatment before any NV has limited efficacy in mitigating NV, while treatment after peak NV exhibits no statistically significant effect but with a trend to exacerbating NV. Optimally timed topical dexamethasone suppression of NV in OIR is associated with increased retinal mitochondrial gene expression and a decrease in inflammatory markers predominantly expressed in immune cells. This study provides new insights into topical steroid effects in retinal NV and into mitochondrial function in phase II ROP, and suggests a simple approach to preventing severe ROP.

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Project description:Although the impact of circadian disruption is well recognized, definitive indicators and time windows for its detection are currently lacking. Here, by conducting transcriptomic, metabolomic, and integrated analysis, we comprehensively investigated the gene and metabolite changes on the 7th day after a single 6-hour phase advance jet lag in mice. Our findings revealed significant alterations during this post-jet lag window, especially in core clock genes Bmal1 and Cry1, and metabolites L-Arginine and SM(d18:1/18:1(11Z)), with notable differences at Zeitgeber Time 0 (ZT0), suggesting ZT0 as a key diagnostic time point. Additionally, we identified L-Serine as a potential biomarker for indexing circadian disruption irrespective of time points. Our study provides new insights into potential biomarkers for detecting circadian clock disruption.

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Project description:Timed sleep restriction designed to mimic human shift work was performed over a 2 week period in mice. On the final day, MBH biopsies were collected at 6 hour intervals to exmaine the effects of sleep restriction on circadian gene expression. (MBH = mediobasal hypothalamus)

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