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RNAseq analysis of genes differentially expressed in H1299 cells with anti-circadian rhythm dysfunctional treatment

ABSTRACT: We examined the biological difference between H1299 cells with the treatments targeting circadian rhythm in order to better understand circadian rhythm disruption as a feature of cancer. To this end, we knocked down CLOCK using siRNA (siCLOCK) or melatonin pre-treatment and assessed the gene expression pattern by RNA-Seq.

ORGANISM(S): Homo sapiens

PROVIDER: GSE196848 | GEO | 2022/02/19

REPOSITORIES: GEO

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RNAseq analysis of genes differentially expressed in H1299 cells with anti-circadian rhythm dysfunctional treatment

Project description:RNAseq analysis of genes differentially expressed in H1299 cells with anti-circadian rhythm dysfunctional treatment

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Project description:Regulatory T cells (Treg cells) are important to maintain self-tolerance. In tissues, Treg cells can perform non-classical functions, for example, they are implicated in regulating metabolic processes in the adipose tissue. Their function in the liver is less well understood. We found here that Treg cells are important to secure the peripheral hepatic circadian rhythm of core-clock regulators and clock-controlled genes. Undisturbed metabolism in the liver required the presence of Treg cells and was especially important in the early postnatal phase, a distinct time period at around day 10, when the liver had not fully matured and Treg cells proliferated and accumulated in the liver-tissue. Our findings highlight a critical role for Treg cells to establish and maintain liver homeostasis.

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Bi-directional regulation between circadian rhythm and neurodegeneration-associated FUS

Project description:Circadian rhythms are daily physiological and behavioral changes governed by an internal molecular clock, and dysfunctions in circadian rhythms have long been associated with various neurodegenerative diseases. Abnormal sleep-wake cycle often precedes the onset of cognitive and motor symptoms in patients, while the pathological changes may further exacerbate the disturbance in circadian cycle. It is unclear whether dysregulated circadian rhythm is a consequence of, or a contributing factor for, neurodegeneration. In addition, the evidence directly connecting the neurodegeneration-associated proteins to core circadian clock gene expression remains sparse. Here we show that FUS, a RNA-binding protein implicated in the pathogenesis of ALS and frontotemporal dementia, exhibits a bi-directional regulation with circadian rhythm. Our meta-analysis of RNAseq datasets and subsequent biochemical analysis revealed FUS as a gene regulated by circadian oscillation. Furthermore, NR1D1 binds the FUS promoter and regulates the amplitude of FUS oscillation. Meanwhile, FUS is recruited by transcriptional co-repressor PSF, and is found in the same complex as Bmal-Clock to repress Per2 expression. More strikingly, in cells and brain tissues from homozygous knock-in rats, the pathogenic R521C mutant FUS significantly alters the oscillation patterns of core circadian genes even at young age. Therefore, our results have revealed a novel bi-directional mechanism whereby dysregulated circadian clock and FUS expression may exacerbate neurodegeneration via mutual influence.

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Circadian rhythm in NIH3T3 cells

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Circadian rhythm in NIH3T3 cells

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