Genes relevant to tissue response to cancer therapy display diurnal variation in mRNA expression in human oral mucosa
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE186805 | GEO | 2021/10/31
REPOSITORIES: GEO
Similar Datasets
Project description:Investigation of transcriptome dynamics of Japanese cedar (Cryptomeria japonica) in winter (Dec. 22-23, 2011) and summer (July 30-31, 2012). We investigated seasonal and diurnal transcriptome dynamics of Japanese cedar (Cryptomeria japonica) by analyzing shoot samples collected at four-hour interval for two days in winter and summer, respectively. We first collected sequence data of expressed genes from shoots to designed microarray probes. Microarray analysis revealed the significant difference of transcripts between summer and winter, and the diurnal transcriptome dynamic in summer.Statistical analysis indicated that about 7.7 % of unique genes showed diurnal rhythms with more than two-fold of peak-to-trough amplitude in summer.
2014-09-29 | GSE53945 | GEO
Project description:To address whether changes in gene expression in blood cells with sleep loss are different in individuals resistant and sensitive to sleep deprivation (SD). Blood draws every 4 hours during a 3-day study: 24-hour normal baseline, 38 hours of continuous wakefulness and subsequent recovery sleep, for a total of 19 time-points per subject, with every 2-hr psychomotor vigilance test (PVT) assessment when awake. Fourteen subjects who were previously identified as behaviourally resistant (n=7) or sensitive (n=7) to SD by PVT. Intervention consisted of 38 hours continuous wakefulness. We found 4,481 unique genes with a significant 24-hour diurnal rhythm during a normal sleep-wake cycle in blood (false discovery rate [FDR] <5%). Biological pathways were enriched for biosynthetic processes during sleep. After accounting for circadian effects, two genes (SREBF1 and CPT1A, both involved in lipid metabolism) exhibited small, but significant, linear changes in expression with the duration of SD (FDR<5%). The main change with SD was a reduction in the amplitude of the diurnal rhythm of expression of normally cycling probe sets. This reduction was noticeably higher in behaviourally resistant subjects than sensitive subjects, at any given p-value. Furthermore, blood cell type enrichment analysis showed that the expression pattern difference between sensitive and resistant subjects is mainly found in cells of myeloid origin, such as monocytes. Individual differences in behavioural effects of sleep deprivation are associated with differences in diurnal amplitude of gene expression for genes that show circadian rhythmicity.
2014-10-02 | GSE56931 | GEO
Project description:Investigation of transcriptome dynamics of Japanese cedar (Cryptomeria japonica) in winter (Dec. 22-23, 2011) and summer (July 30-31, 2012). We investigated seasonal and diurnal transcriptome dynamics of Japanese cedar (Cryptomeria japonica) by analyzing shoot samples collected at four-hour interval for two days in winter and summer, respectively. We first collected sequence data of expressed genes from shoots to designed microarray probes. Microarray analysis revealed the significant difference of transcripts between summer and winter, and the diurnal transcriptome dynamic in summer.Statistical analysis indicated that about 7.7 % of unique genes showed diurnal rhythms with more than two-fold of peak-to-trough amplitude in summer. Summer samples were collected at four-hour interval for two days (12 time points) from three different cuttings as biological repeats (total 36 samples). Winter samples were collected at 4:00/8:00/12:00/16:00/20:00/24:00 on Dec 22 and 12:00/24:00 on Dec 23 (total eight samples).
2014-09-29 | E-GEOD-53945 | biostudies-arrayexpress
Project description:BackgroundTo address a critical gap for application of cancer chronotherapy of when would be the best time(s) for treating an individual cancer patient, we conducted a pilot study to characterize diurnal variations of gene expression in oral mucosal tissue, which is vulnerable to damage from cancer therapies.MethodsWe conducted RNA-seq assay on individual oral mucosal samples collected from 11 healthy volunteers every 4 hours (6 time points). Using a cosine-based method, we estimated the individual and average values of peak-time and amplitude for each gene. Correlations between gene expression peak-times and age was examined, adjusting for individual's sleep timing.ResultsAmong candidate gene pathways that are relevant to treatment response, 7 of 16 genes (PER3, CIART, TEF, PER1, PER2, CRY2, ARNTL) involved in circadian regulation and 1 of 118 genes (WEE1) involved in cell cycle regulation achieved p-value ≤ 0.1 and relative amplitude>0.1. The average peak times were approximately 10:15 for PER3, CIART and TEF, 10:45 for PER1, 13:00 for WEE1, PER2 and CRY2, and 19:30 for ARNTL. Ranges in peak times across individuals differed by gene (e.g., 8 hours for PER1; 16.7 hours for WEE1). Older people had later peak times for PER1 (r = 0.77, p = 0.03) and PER3 (r = 0.69, p-value = 0.06).ConclusionIn oral mucosa, expression of some genes relevant to treatment response displayed diurnal variation. These genes may be candidates for development of biomarkers for optimizing individual timing of cancer therapy using non-invasively collected oral mucosa.
| S-EPMC8231453 | biostudies-literature
Project description:The circadian clock drives daily changes of physiology, including sleep-wake cycles, by regulating transcription, protein abundance and function. Circadian phosphorylation controls cellular processes in peripheral organs, but little is known about its role in brain function and synaptic activity. We applied advanced quantitative phosphoproteomics to mouse forebrain synaptoneurosomes isolated across 24h, accurately quantifying almost 8,000 phosphopeptides. Remarkably, half of the synaptic phosphoproteins, including numerous kinases, had large-amplitude rhythms peaking at rest-activity and activity-rest transitions. Bioinformatic analyses revealed global temporal control of synaptic function via phosphorylation, including synaptic transmission, cytoskeleton reorganization and excitatory/inhibitory balance. Remarkably, sleep deprivation abolished 98% of all phosphorylation cycles in synaptoneurosomes, indicating that sleep-wake cycles rather than circadian signals are main drivers of synaptic phosphorylation, responding to both sleep and wake pressures.
2019-10-14 | PXD010697 | Pride
Project description:22 healthy volunteers without sleep disorders were resident in an environmental scheduling facility and participated in a forced-desynchrony protocol, in which the sleep-wake cycle and the associated fasting-feeding cycle is scheduled to a 28-hour period, of which one third (i.e. 9h 20min) is scheduled for sleep. Under these conditions, during which light levels in the waking episode are kept low and sleep is scheduled in darkness, the phase of the melatonin rhythm occurred at approximately the same clock time during the first (D1) and fourth (D4) 28-h cycle and there were no major changes in either the amplitude or the waveform of this rhythm. During D1 and D4 7 blood samples were taken, RNA was extracted from leukocytes, labelled and hybridised to human whole-genome microarrays A total of 287 samples comprising 22 human subjects, for which 14 samples across multiple time-points/sleep condition were collected.
2014-01-23 | E-GEOD-48113 | biostudies-arrayexpress
Project description:Microglia cells are the innate immune cells of the brain. They are increasingly studied for their role in virtually all pathological events in the central nervous system. However, no study has thus far looked at whether microglia cells undergo wake and sleep state-dependent changes in transcriptional and translational profile. Rodents are nocturnal animals, and most studies are investigating microglia cells during the rodent's sleep phase, hence during the day, for translational purposes. The aim of this study was to compare the microglial transcriptional, translational and functional profile between the wake and sleep phase. Our results provide evidence that the innate immune cells of the brain do undergo a transcriptional and translational adaptation to the wake or sleep state.
2022-11-02 | GSE200314 | GEO
Project description:To address whether changes in gene expression in blood cells with sleep loss are different in individuals resistant and sensitive to sleep deprivation (SD). Blood draws every 4 hours during a 3-day study: 24-hour normal baseline, 38 hours of continuous wakefulness and subsequent recovery sleep, for a total of 19 time-points per subject, with every 2-hr psychomotor vigilance test (PVT) assessment when awake. Fourteen subjects who were previously identified as behaviourally resistant (n=7) or sensitive (n=7) to SD by PVT. Intervention consisted of 38 hours continuous wakefulness. We found 4,481 unique genes with a significant 24-hour diurnal rhythm during a normal sleep-wake cycle in blood (false discovery rate [FDR] <5%). Biological pathways were enriched for biosynthetic processes during sleep. After accounting for circadian effects, two genes (SREBF1 and CPT1A, both involved in lipid metabolism) exhibited small, but significant, linear changes in expression with the duration of SD (FDR<5%). The main change with SD was a reduction in the amplitude of the diurnal rhythm of expression of normally cycling probe sets. This reduction was noticeably higher in behaviourally resistant subjects than sensitive subjects, at any given p-value. Furthermore, blood cell type enrichment analysis showed that the expression pattern difference between sensitive and resistant subjects is mainly found in cells of myeloid origin, such as monocytes. Individual differences in behavioural effects of sleep deprivation are associated with differences in diurnal amplitude of gene expression for genes that show circadian rhythmicity. Blood draws were done every 4 hours during a 3-day (+1 baseline day) study: 24-hour normal baseline (6 time points: day 1 8hr, 12hr, 16hr, 20hr, day 2 0hr, 4hr), 38 hours of continuous wakefulness (10 time points: day 2 8hr, 12hr, 16hr, 20hr, day 3 0hr, 4hr, 8hr, 12hr, 16hr, 20hr) and subsequent recovery sleep (3 time points: day 4 0hr, 4hr, 8hr), for a total of 19 time-points per subject, with every 2-hr psychomotor vigilance test (PVT) assessment when awake. The missing/failed samples were as following: Resistant subjects (total 10 samples): BH006 day 2 20hr, 12hr, BH003 day 2 12hr, 4hr, BH003 day 3 4hr, BH008 day 4 0hr, BH008 day 1 16hr, BH008 day 3 16hr 20hr, BH010 day 4 0hr; Sensitive subjects (total 7 samples): BH004 day 2 12hr and 1 more missing sample, BH026 day 2 4hr, BH007 day 2 20hr and 1 more missing sample, BH016 day 2 4hr, BH015 day 3 0hr.
2014-10-02 | E-GEOD-56931 | biostudies-arrayexpress
Project description:Inadequate sleep prevails in modern society and it impairs the circadian transcriptome. However, whether acute sleep deprivation has impact on the circadian rhythms is not clear. Here, we show that in mouse lung, a 10-hour acute sleep deprivation can alter the circadian expression of approximally 3,000 genes. We found that circadian rhythm disappears in genes related to metabolism and signaling pathways regulating protein phosphorylation after acute sleep deprivation, while the core circadian regulators do not change much in rhythmicity. Importantly, the strong positive correlation between mean expression and amplitude (E-A correlation) of cycling genes has been validated in both control and sleep deprivation conditions, supporting the energetic cost optimization model of circadian gene expression. Thus, we reveal that acute sleep deprivation leads to a profound change in the circadian gene transcription that influences the biological functions in lung.
2021-02-09 | GSE166335 | GEO
Project description:Circadian dysregulation associates with numerous diseases including metabolic dysfunction, sleep disorder, depression and aging. Given that declined circadian amplitude is a trait commonly found with compromised health, interventions that design in precluding circadian amplitude from dampening will aid to mitigate complex, circadian-related diseases. Here we identify a neurogenic small molecule ISX-9 that is able to support persistent and higher amplitude of circadian oscillations. ISX-9 improves diurnal metabolic rhythms in middle-aged mice. Moreover, the ISX-9-treated mice show better sleep homeostasis with increased delta power during the day time and higher locomotive activity in the dark period. ISX-9 augments CaMKIIδ expression and increases BMAL1 activity via eliciting CaMKIIδ-mediated phosphorylation on BMAL1 residues S513/S515/S516, accordingly composes a positive feedback effect on enhancing circadian amplitude. CaMKIIδ-targeting, and the use of ISX-9 may serve as decent choices for treating circadian-related disorders.
2022-06-06 | PXD034339 |