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RNA sequencing of livers from Per2-/- and WT mice following MC38 cancer cells injection reveals transcriptional differences as early as 7 days post injection

ABSTRACT: RNA sequencing of livers from Per2-/- and WT mice following MC38 cancer cells injection reveals transcriptional differences as early as 7 days post injection

PROVIDER: PRJNA658002 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12474904_1.fastq.gz	Fastqsanger.gz
	SRR12474904_2.fastq.gz	Fastqsanger.gz
	SRR12474905_1.fastq.gz	Fastqsanger.gz
	SRR12474905_2.fastq.gz	Fastqsanger.gz
	SRR12474906_1.fastq.gz	Fastqsanger.gz

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RNA sequencing of livers from Per2-/- and WT mice following MC38 cancer cells injection reveals transcriptional differences as early as 7 days post injection

Project description:The circadian clock regulates diverse physiological processes by maintaining a 24-hour gene expression pattern. Genetic and environmental cues that disrupt normal clock rhythms can lead to cancer, yet the extent to which this effect is controlled by the cancer cells versus non-malignant cells in the tumor microenvironment (TME) is not clear. Here we set out to address this question, by selective manipulation of circadian clock genes in the TME. In two different mouse models of cancer we find that expression of the core clock gene Per2 in the TME is crucial for tumor initiation and metastatic colonization, whereas another core gene, Per1, is dispensable. We further show that loss of Per2 in the TME leads to significant transcriptional changes in response to cancer cell introduction. These changes may contribute to a tumor-suppressive microenvironment. Thus, our work unravels an unexpected protumorigenic role for the core clock gene Per2 in the TME, with potential implications for therapeutic dosing strategies and treatment regimens.

2020-10-15 | GSE156450 | GEO

Microarray of MC38-R tumors following intratumoral injection of IL-12 mRNA or control mRNA

Project description:We designed a novel intratumoral (IT) IL-12 mRNA therapy to promote local IL-12 tumor production whilst mitigating systemic effects. A single IT dose of mouse (m)IL-12 mRNA induced IFNγ and CD8+ T cell-dependent tumor regression in multiple syngeneic mouse models including MC38-R, and animals with a complete response demonstrated immunity to re-challenge. In order to further investigate the impact of mIL-12 mRNA on the MC38-R TME, we performed tumor transcriptomic evaluation 24h and 7 days after a single IT dose of 0.5 micrograms IL-12 or control mRNA. mRNA was isolated from snap-frozen syngeneic tumors using an RNeasy mini kit (Qiagen) and quantified on the Affymetrix mouse 430 2.0 microarray.

2020-09-01 | E-MTAB-9316 | biostudies-arrayexpress

Intratumoral injection of CpG1826

Project description:To determine the effect on gene expression of intratumoral injection of the Toll-like receptor agonist CpG1826. MC38 colon cancer cells were injected subcutaneously into C57BL/6 mice and allowed to establish until ~40 mm2.

2009-09-23 | GSE18203 | GEO

Negative reciprocal regulation between Sirt1 and Per2 modulates the circadian clock and aging (microarray expression)

Project description:Sirtuin 1 (SIRT1) is involved in both aging and circadian-clock regulation, yet the link between the two processes in relation to SIRT1 function is not clear. Using Sirt1-deficient mice, we found that Sirt1 and Period 2 (Per2) constitute a reciprocal negative regulation loop that plays important roles in modulating hepatic circadian rhythmicity and aging. Sirt1-deficient mice exhibited profound premature aging and enhanced acetylation of histone H4 on lysine16 (H4K16) in the promoter of Per2, the latter of which leads to its overexpression; in turn, Per2 suppresses Sirt1 transcription through binding to the Sirt1 promoter at the Clock/Bmal1 site. This negative reciprocal relationship between SIRT1 and PER2 was also observed in human hepatocytes. We further demonstrated that the absence of Sirt1 or the ectopic overexpression of Per2 in the liver resulted in a dysregulated pace of the circadian rhythm. The similar circadian rhythm was also observed in aged wild type mice. The interplay between Sirt1 and Per2 modulates aging gene expression and circadian-clock maintenance. To investigate hepatic SIRT1-dependent aging related genes, livers from wild type mice at 3 months (young), 12 months (middle age), and 19 months (old) of age, as well as Sirt1-deficient mice at 3 months of age were snap frozen and subject to RNA isolation and microarray analysis.

2016-08-08 | E-GEOD-54436 | biostudies-arrayexpress

Cry1 and Per2 protein complex in mouse liver

Project description:This project aimed to profile interacting proteins of Cry1 and Per2 from mouse liver.

2023-03-11 | PXD037841 | Pride

RNA-seq of parental MC38 and anti-PD-1 resistant MC38 subcutaneous tumors

Project description:MC38 tumors resistant to anti-PD-1 treatment (MC38-resistant) were generated through serial in vivo passaging, and global gene expression analysis was used to compare resistant and parental tumors. MC38 and MC38-resistant tumors exhibited widespread changes in global gene expression.

2021-07-22 | GSE180309 | GEO

Immunopeptidome on MC38 Cell line

Project description:PTM – driven antigenicity – immunopeptidome of MC38 cell line

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ASS lime injection - injection site

Project description:ASS lime injection - injection site

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PER2 synchronizes mitotic expansion and decidual transformation of human endometrial stromal cells

Project description:Implantation is dependent on synchronized interactions between the conceptus and surrounding decidual cells but the involvement of clock genes in this process is not well understood. Circadian oscillations are predicated on transcriptional-translational feedback loops, which balance the activities of the transcriptional activators CLOCK and BMAL1 and repressors encoded by PER and CRY genes. Here we show that loss of PER2 expression silences circadian oscillations in decidualizing human endometrial stromal cells (HESCs). Downregulation was preceded by reduced CLOCK binding to a noncanonical E-box enhancer in the PER2 promoter and occurred between 12 - 24 h after exposure to a deciduogenic stimulus. RNA sequencing revealed that premature inhibition of PER2 by siRNA knockdown leads to a grossly disorganised decidual response. Gene ontology analysis highlighted a preponderance of cell cycle regulators amongst the 1,121 genes perturbed upon PER2 knockdown. Congruently, PER2 inhibition abrogated mitotic expansion of differentiating HESCs by inducing cell cycle block at G2/M. Analysis of mid-luteal endometrial biopsies revealed an inverse correlation between PER2 transcript levels and the number of miscarriages in women suffering reproductive failure. Thus, PER2 synchronizes mitotic expansion of HESCs with a periodic decidual gene expression; uncoupling of these events may cause persistent pregnancy failure. Endometrial mRNA profiles of paired control (siRNA-NT) and siRNA-PER2 were generated by deep sequencing, in triplicate using Illumina

2015-09-16 | E-GEOD-62854 | biostudies-arrayexpress

Genome-wide analysis of PER2 on BMAL1 DNA binding and transcription

Project description:We use PER2-inducible system to analyse BMAL1 chromatin binding by ChIPseq and expression profile by mRNA-Seq. PER2 decrease BMAL1 chromatin bindging but the effect on transcrtipion is gene-specific.

2017-01-10 | GSE93318 | GEO

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