ATAC-Seq of liver in cancer cachexia
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE293099 | GEO | 2025/07/20
REPOSITORIES: GEO
Similar Datasets
Project description:To study the response in the liver to cachectic and weight-stable cancer, we performed RNA-sequencing of whole liver nuclei and hepatocyte nuclei that were isolated using the INTACT methodology of weight stable NC26, pre-cachectic C26, cachectic C26, weight-stable MC38 and cachectic 8025 tumor bearing mice as well as their respective PBS controls.
2025-07-20 | GSE293096 | GEO
Project description:Analysis of gene expression in CD2F1 mice with cancer cachexia due to implantation of C26 colon carcinoma cells. Total RNA obtained from quadriceps muscle of female CD2F1 mice with early weight loss (10%) or severe weight loss (15%) due to intrascapular subcutaneous implantation of one million C26 colon adenocarcinoma cells.
2011-08-29 | E-GEOD-24112 | biostudies-arrayexpress
Project description:Forkhead BoxO (FoxO) transcription factors expressed in adult skeletal muscle promote muscle atrophy during various catabolic conditions. We have identified the genome wide target genes and biological networks regulated by FoxO in skeletal muscle during Colon-26 (C-26) cancer cachexia. In this dataset, we include the expression data obtained from the tibialis anterior muscles of control and severely cachectic Colon-26 mice in which FoxO-dependent transcription was either intact (AAV9-EV) or inhibited (AAV9-d.n.FoxO). These data were used to obtain 543 FoxO target genes during cancer. These target genes were identified as those genes whose expression was both differentially regulated in skeletal muscle in response to cancer (control AAV9-EV vs. C26 AAV9-EV), and differentially regulated in the presence of d.n.FoxO (C26 AAV9-EV vs. C26 AAV9-d.n.FoxO).
2014-12-31 | GSE56555 | GEO
Project description:Cancer cachexia (CC) is a poorly understood cause of morbidity and mortality, which has no efficacious treatment or generally-accepted management strategy. The consensus definition for CC identified skeletal muscle loss as a key marker in the diagnosis and classification of cachexia. The importance of fat wasting however, is less understood. During cachexia, different adipose depots demonstrate differential wasting rates. Studies from animal models have suggested adipose tissue may be a key driver of muscle wasting through fat-muscle crosstalk but human studies in this area are lacking. We performed global gene expression profiling of intra-abdominal (IAAT) and subcutaneous (SAT) adipose from weight stable and cachectic cancer patients and healthy controls. Cachexia was defined as >2% weight loss plus low CT-muscularity. Biopsies of SAT and IAAT were taken from patients undergoing resection for oesophago-gastric cancer, and healthy controls (donor nephrectomy) (n=16 and 8 respectively). RNA was isolated and reverse transcribed. cDNA was hybridised to the Affymetrix Clariom S Microarray and data was analysed using R/Bioconductor. Differential expression of genes was assessed using empirical Bayes and moderated-t-statistic approaches. Category enrichment analysis was used with a tissue-specific background to examine the biological context of differentially expressed genes. Selected differentially regulated genes were validated by qPCR. ELISA for Intelectin-1 was performed on IAAT samples for the corresponding patients. The current cohort plus 12 additional patients from each group also had plasma Intelectin-1 ELISA carried out. In IAAT versus SAT comparisons there were 2101, 1722 and 1659 significantly regulated genes in the cachectic, weight stable and control groups respectively. There were 2200 significantly regulated genes from IAAT in cachectic patients compared to controls and 1253 significantly regulated genes from IAAT in weight stable cancer patients compared to controls. The gene showing the largest difference in expression was Intelectin-1 (Omentin-1) (FDR corrected p=0.0001); a novel adipocytokine associated with weight loss in other groups. Genes involving inflammation were enriched in cancer and control IAAT versus SAT though different groups of genes contributed. Energy metabolism and fat browning genesets were downregulated in cancer IAAT as were key fat browning genes (e.g. UCP1). SAT and IAAT have unique gene expression signatures. IAAT is metabolically active in cancer, and maybe a target for therapeutic manipulation. IAAT may play a fundamental role in cachexia, but the downregulation of energy metabolism genes implies a limited role for fat browning in human cachectic patients, in contrast to pre-clinical models.
2020-05-29 | GSE131835 | GEO
Project description:To study the differentially regulated genes in cachectic mice, we RNA sequenced the TA muscles of different mouse models of cachexia and their respective controls
2025-03-01 | GSE227486 | GEO
Project description:We evaluated the transcriptional response in the heart upon hepatocyte-specific overexpression of REV-ERBα in the C26 cancer cachexia model.
2025-07-20 | GSE293093 | GEO
Project description:Mice were eithier injected with LLC or C26 cells, or injected with tamoxifen to indcue pancratic cancer in the KPP model. Matched controls were injected with PBS to mimic cell injections and control mice were injected with tamoxifen as controls for KPP.
2024-08-01 | GSE245208 | GEO
Project description:Cachexia is an exacerbating event in many types of cancer that is strongly associated with a poor prognosis. We have identified cytokine, signaling and transcription factors that are required for cachexia in the mouse C26 colon carcinoma model of cancer. C2C12 myotubes treated with conditioned medium from C26 cancer cells induced atrophy and activated a STAT-dependent reporter gene but not reporter genes dependent on SMAD, FOXO, C/EBP, NF-ĸB, or AP-1. Of the gp130 family members IL-11, IL-6, oncostatin M (OSM), and leukemia inhibitory factor (LIF), only OSM and LIF were sufficient to activate the STAT reporter in myotubes. A LIF blocking antibody abolished C26 CM-induced STAT reporter activation STAT3 phosphorylation and myotube atrophy, but blocking antibodies to IL-6 or OSM did not. JAK2 inhibitors also blocked the C26 CM-induced STAT reporter activation, STAT3 phosphorylation, and atrophy in myotubes. LIF at levels found in the C26 CM was sufficient for STAT reporter activation and atrophy in myotubes. In vivo, an increase in serum LIF preceded the increase in IL-6 in mice with C26 tumors. Overexpression of a dominant negative Stat3Cβ-EGFP gene in myotubes and in mouse muscle blocked the atrophy caused by C26 CM or C26 tumors, respectively. Taken together these data support an important role of LIF- JAK2-STAT3 in C26 cachexia and point to a therapeutic approach for at least some types of cancer cachexia. from three replicate wells of cells at each treatment, pools of total RNA were used to create cDNA which were evaluated on Affymetrix mouse gene 1.0 ST v.1 arrays.
2015-06-25 | E-GEOD-68827 | biostudies-arrayexpress
Project description:Background: MicroRNAs (miRs) are small non-coding RNAs that regulate gene (mRNA) expression. Although pathological role of miRs have been studied in muscle wasting conditions such as age, obesity, starvation and muscular dystrophy, their roles in Cancer Cachexia CC are still emerging. Objectives: (i) to profile human skeletal muscle expressed miRs; (ii) to identify differentially expressed (DE) miRs between cachectic and non-cachectic cancer patients; (iii) to identify mRNA targets for the DE miRs to gain mechanistic insights and (iv) to investigate if miRs show potential prognostic and predictive value. Methods: 43 cancer patients were included, of which 19 were cachectic cases exhibiting pre-illness weight loss ≥ 5% and 24 non-cachectic cancer controls who were weight stable in the preceding 6 months. Total RNA isolated from muscle biopsies were subjected to next generation sequencing (NGS). Results: 781 miRs were profiled and 82 miRs with read counts of ≥ 5 in 80% of samples were retained for analysis. We identified 7 DE miRs (up-regulated, fold change of ≥1.4 at p< 0.05). Potential mRNA targets for the DE miRs were identified using previously described human skeletal muscle mRNA expression data (n=90) and identified 212 potential mRNA targets. Ingenuity Pathway Analysis identified 41 pathways (p<0.05) including pathways of myogenesis and inflammation. qRT-PCR analysis of representative miRs, showed similar direction of effect (p<0.05) as in NGS. And lastly, we evaluated the identified miRs for prognostic and predictive value. Conclusions: We identified seven novel miRs associated with CC and pathways that are regulated in CC.
2017-01-09 | GSE75473 | GEO
Project description:Cancer cachexia has been linked to gut bacterial alterations, but alterations of gut viruses, mostly bacteriophages, have not yet been explored. We performed shotgun metagenomic sequencing of DNA from stool samples of 78 cachectic and 42 non-cachectic cancer patients. K-mer-based matching to reference databases revealed abundance variations of bacteria and viruses. Beyond bacterial alterations, cachectic patients exhibited significantly lower bacteriophage abundance, predominantly affecting Caudovirales and Siphoviridae species (double-stranded DNA) but also Inoviridae and Microviridae families (single-stranded DNA).
| EGAS00001007156 | EGA