Microarray analysis of colon carcinoma cell lines
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE46549 | GEO | 2014/05/31
SECONDARY ACCESSION(S): PRJNA200953
REPOSITORIES: GEO
Similar Datasets
Project description:To investigate potential differences between strong and weak oscillators at the gene expression level we carried out a transcriptome analysis for each cell line. Our results indicate that phenotypic circadian clock differences are reflected by gene expression differences both in genes of the core network, but also in additional genes not directly associated with circadian clock functions. We carried out a gene expression analysis of 6 colon cancer cell lines (HCT116, HT-29, RKO, SW480, LIM1512 and CaCo2) for each the RNA was collected at two time points (0hr and 48 hr after syncronization). As a reference the osteosarcoma U2OS cell line was used. No treatment was applied.
2014-05-31 | E-GEOD-46549 | biostudies-arrayexpress
Project description:In mammalian tissues circadian gene expression can be driven by local oscillators or systemic signals controlled by the master pacemaker in the suprachiasmatic nucleus. Here we show that simulated body temperature cycles, but not peripheral oscillators, can control the rhythmic expression of Cold-Inducible RNA binding Protein (CIRP) in cultured fibroblasts. In turn, loss-of-function experiments indicate that CIRP is required for high amplitude circadian gene expression. The transcriptome-wide identification of CIRP-bound RNAs by a biotin-streptavidin based CLIP-seq procedure revealed several CIRP-bound transcripts encoding circadian oscillator proteins. One of these, CLOCK, accumulated to particularly low levels in CIRP-depleted fibroblasts. Since ectopic expression of CLOCK improved circadian gene expression in these cells, we surmise that CIRP confers robustness to circadian oscillators via the regulation of CLOCK expression. Identification of CIRP-interacting RNA molecules in NIH3T3 cells and RNA expression in NIH3T3 cells treated with Control or CIRP siRNA after incubation of the cells at 33M-BM-0C for 8 hours
2012-08-24 | E-GEOD-37685 | biostudies-arrayexpress
Project description:In mammalian tissues circadian gene expression can be driven by local oscillators or systemic signals controlled by the master pacemaker in the suprachiasmatic nucleus. Here we show that simulated body temperature cycles, but not peripheral oscillators, can control the rhythmic expression of Cold-Inducible RNA binding Protein (CIRP) in cultured fibroblasts. In turn, loss-of-function experiments indicate that CIRP is required for high amplitude circadian gene expression. The transcriptome-wide identification of CIRP-bound RNAs by a biotin-streptavidin based CLIP-seq procedure revealed several CIRP-bound transcripts encoding circadian oscillator proteins. One of these, CLOCK, accumulated to particularly low levels in CIRP-depleted fibroblasts. Since ectopic expression of CLOCK improved circadian gene expression in these cells, we surmise that CIRP confers robustness to circadian oscillators via the regulation of CLOCK expression.
2012-08-24 | GSE37685 | GEO
Project description:The mammalian circadian timing system consists of a master pacemaker in the suprachiasmatic nucleus (SCN) that synchronizes self-sustained oscillators in most peripheral cells. Rhythmic gene expression in peripheral tissues can be driven by cyclic systemic cues emanating from the SCN or by local oscillators. To discriminate between these two mechanisms, we engineered a mouse strain with a conditionally active liver clock. Transcriptome profiling revealed that the circadian transcription of most genes depends on functional hepatocyte clocks. However, the expression of 31 genes, including mPer2, oscillates robustly in clock-arrested hepatocytes. Such genes may be implicated in the synchronization of liver oscillators
2006-12-30 | E-MEXP-842 | biostudies-arrayexpress
Project description:Intercellular coupling is crucial to prevent desynchronization of cell-autonomous oscillator networks and thus, the disruption of circadian tissue functions. While, neuronal oscillators within the mammalian central clock, the suprachiasmatic nucleus (SCN), couple intercellularly via the exchange of secreted neurotransmitters, intercellular coupling among peripheral oscillators is highly debated and molecular mechanisms are unknown. In our study, we show that peripheral circadian oscillators couple intercellularly via the exchange of secreted signaling molecules and identify TGF-beta as peripheral coupling factor. TGF-beta signaling induces the cAMP response element dependent, immediate-early expression of the clock gene PER2, thereby phase-adjusting the molecular circadian oscillator. Genetic or pharmacologic disruption of TGF-beta signaling causes desynchronization of cellular oscillators resulting in amplitude reduction and increased sensitivity towards Zeitgeber cues. Our findings reveal a previously unknown mechanism of peripheral coupling and open a new perspective on the importance of peripheral clock synchrony for rhythmic organ functions and circadian health.
2021-07-23 | GSE158577 | GEO
Project description:Circadian clocks are endogenous oscillators that drive organismal metabolism and physiology. Here, we report the first global in vivo quantification of circadian phosphorylation rhythms in mammals. Of more than 20,000 in vivo phosphosites, 25% significantly oscillate in the mouse liver, including novel sites on core clock proteins. Analyzing kinase substrate motifs, we find that the EGF/RAS/ERK pathway is predominantly activated during the day and the AKT/mTOR/p70S6K at night. The extent and amplitude of phosphorylation cycles dominate the rhythms of transcript and protein abundance. A dominant regulatory role for phosphorylation-dependent circadian tuning of signaling pathways allows the organism to rapidly and economically respond to daily changes in nutrient availability and integrate different signaling triggers.
2016-10-18 | PXD003751 | Pride
Project description:There is growing appreciation that the feeling of well-being, alterations in mood and susceptibility to a variety of medical disorders depend on the proper expression of the master circadian clock and the synchrony among the other oscillators found in many peripheral tissues. To improve our understanding of the role of peripheral oscillators, an improved understanding of the molecular machinery sub-serving the circadian variation in gene expression is essential. Our long-term goal is to understand the molecular mechanisms that initiate circadian gene expression following external stimulation in the mammalian pineal gland. Are all or just some of the "circadian clock" genes induced by NE, cAMP, or cGMP? In this project we compare a series of gene expression patterns using DNA microarray in response to cAMP, cGMP and NE stimulation to understand why NE does not initiate circadian rhythms in the rat pineal gland. As a preliminary experiment we will compare gene expression 0, 1, and 4 h after start of chemical stimulation. A failure of NE to initiate circadian rhythms is due to failure of activation of certain "circadian clock" genes. We found that circadian rhythms are initiated by stimulation of cAMP or cGMP analogue in the rat pineal gland, while norepinephrine (NE) stimulation only moderately induce Period1 mRNA (one of "circadian clock" genes) 24 h after start of stimulation. From these results we hypothesize that external stimulation activates some "circadian clock" genes simultaneously, and that failure of circadian rhythm initiation following NE stimulation is due to insufficient "circadian clock" genes activations. Male rats of wistar strain are kept in 12h-12h light dark cycles at least for one week before start of experiments. Pineal glands are removed from animals and placed in the culture dish. Rat pineal glands are cultured for 3 days before chemical stimulation. On the day of experiment, the pineal cultures are stimulated using one of NE, cAMP and cGMP analogues for 1 or 4 h before harvest. The samples are immediately frozen and total RNA are extracted from each group which are from a pool of 8 pineal glands using Trizol reagent (Invitrogen). Concentrations of total RNA are determined using spectrophotometer, and six microgram of total RNA is aliquoted in each sample tube for further analysis. Since we already have Affymetrix Rat Genome U34A array GeneChips, we would like to send Chips as well as our total RNA samples. Experiment Overall Design: as above
2008-06-12 | E-GEOD-2865 | biostudies-arrayexpress
Project description:Circadian rhythms are responsive to a variety of external cues, light and metabolism being the most important. In mammals, the light signal is sensed by the retina and transmitted to the SCN master clock, where it is translated into the molecular oscillator via regulation of clock gene transcription. The signalling pathways governing the molecular translation from metabolic signals to circadian output in peripheral oscillators, in contrast, are less understood. FOXO transcription factors are known to translate external metabolic cues to internal transcriptional programs. In the past couple of years it has become evident that both FOXO transcription factors and the circadian clock are of key importance in the underlying mechanisms of ageing and the regulation of metabolism. We now show FOXO3 to be a crucial modulator of circadian rhythmicity via direct transcriptional regulation of Clock, a core component of the molecular oscillator, and identify FOXO3 as a novel link in the circadian feedback loop, which is required for circadian rhythms in liver. We propose that FOXO3 directly feeds back into the circadian oscillator in response to metabolic cues.
2014-06-03 | GSE41555 | GEO
Project description:Circadian rhythms are responsive to a variety of external cues, light and metabolism being the most important. In mammals, the light signal is sensed by the retina and transmitted to the SCN master clock, where it is translated into the molecular oscillator via regulation of clock gene transcription. The signalling pathways governing the molecular translation from metabolic signals to circadian output in peripheral oscillators, in contrast, are less understood. FOXO transcription factors are known to translate external metabolic cues to internal transcriptional programs. In the past couple of years it has become evident that both FOXO transcription factors and the circadian clock are of key importance in the underlying mechanisms of ageing and the regulation of metabolism. We now show FOXO3 to be a crucial modulator of circadian rhythmicity via direct transcriptional regulation of Clock, a core component of the molecular oscillator, and identify FOXO3 as a novel link in the circadian feedback loop, which is required for circadian rhythms in liver. We propose that FOXO3 directly feeds back into the circadian oscillator in response to metabolic cues.
2014-06-03 | GSE41554 | GEO
Project description:Circadian clocks are cell-autonomous oscillators regulating daily rhythms in a wide range of physiological, metabolic and behavioral processes. Conversely, metabolic signals such as redox state, NAD+/NADH and AMP/ADP ratios or heme feed back to and modulate circadian mechanisms to optimize energy utilization across the 24-hour cycle. We show that the signaling molecule carbon monoxide (CO) generated by rhythmic heme degradation is required for normal circadian rhythms as well as circadian metabolic outputs. CO suppresses circadian transcription by attenuating CLOCK/BMAL1 binding to target promoters. Pharmacological inhibition or genetic depletion of CO-producing heme oxygenases abrogate normal daily cycles in mammalian cells and Drosophila. In mouse hepatocytes, suppression of CO production leads to a global upregulation of CLOCK/BMAL1-dependent circadian gene expression and thereby misregulation of many metabolic processes including gluconeogenesis.
2016-10-05 | GSE55448 | GEO