Skeletal muscle transcriptome profile in LLC mice model of cancer cachexia.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA604025 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10991590_1.fastq.gz | Fastqsanger.gz | |||
| SRR10991590_2.fastq.gz | Fastqsanger.gz | |||
| SRR10991591_1.fastq.gz | Fastqsanger.gz | |||
| SRR10991591_2.fastq.gz | Fastqsanger.gz | |||
| SRR10991592_1.fastq.gz | Fastqsanger.gz |
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Project description:Cancer cachexia is a metabolic syndrome with alterations in gene expression profile that consequently lead to skeletal muscle wasting. Here, we used RNA sequencing to analyze the mRNA expression profile in the tibialis anterior muscles of the Lewis lung carcinoma (LLC) model of cancer cachexia.
2020-05-19 | GSE144567 | GEO
Project description:Cancer cachexia is a metabolic syndrome with alterations in gene expression profile that consequently lead to skeletal muscle wasting. Here, we used RNA sequencing to analyze the microRNA expression profile in the tibialis anterior muscles of the Lewis lung carcinoma (LLC) model of cancer cachexia.
2020-05-19 | GSE145393 | GEO
Project description:Skeletal muscle transcriptome profile in LLC mice model of cancer cachexia [miRNA-seq]
| PRJNA607068 | ENA
Project description:Background: Cancer cachexia (CAC) reduces patient survival and quality of life. Developments of efficient therapeutic strategies are required for the CAC treatments. This long-term process could be shortened by the drug-repositioning approach which exploits old drugs approved for non-cachexia disease. Amiloride, a diuretic drug, is clinically used for treatments of hypertension and edema due to heart failure. Here, we explored the effects of amiloride for ameliorating muscle wasting in murine models of cancer cachexia. Methods: CT26 and LLC tumor cells were subcutaneously injected into mice to induce cancer cachexia. Amiloride was intraperitoneally injected daily once tumors were formed. Cachexia features of the CT26 and LLC models, respectively, were characterized by phenotypic, histopathologic and biochemical analyses. Plasma exosomes and muscle atrophy-related proteins were quantitatively analyzed. Integrative NMR-based metabolomic and transcriptomic analyses were conducted to identify significantly altered metabolic pathways and distinctly changed metabolism-related biological processes in gastrocnemius. Results: The CT26 and LLC models displayed prominent cachexia features including decreases in body weight, skeletal muscle, adipose tissue and muscle strength. The amiloride treatment in tumor-bearing mice distinctly alleviated muscle atrophy and relieved cachexia-related features without affecting tumor growth. The CT26 and LLC cachexia mice showed increased particle density of plasma exosomes which were largely derived from tumors. Significantly, the amiloride treatment inhibited tumor-derived exosome release, which did not obviously affect exosome secretion from non-neoplastic tissues or induce observable systemic toxicities in normal healthy mice. Integrative-omics revealed significant metabolic impairments in cachectic gastrocnemius, including promoted muscular catabolism, inhibited muscular protein synthesis, blocked glycolysis and impeded ketone body oxidation. The amiloride treatment evidently improved the metabolic impairments in cachectic gastrocnemius. Conclusions: Our results demonstrated the efficacy of amiloride in ameliorating cachectic muscle wasting and elucidated the underlying mechanistic rationale for its use as an alternative strategy to improve CAC treatments.
2021-07-14 | GSE173250 | GEO
Project description:Cancer cachexia is a debilitating metabolic disorder characterized by involuntary loss of body and muscle mass, leading to increased morbidity and mortality. We previously found that Forkhead box P1 (FoxP1) upregulation in skeletal muscle causes muscle wasting and is required for muscle wasting in response to cancer. However, transcriptional networks targeted by FoxP1 in skeletal muscles undergoing cancer-induced wasting remain largely unknown. Here, we identify FoxP1 as a key disruptor of the skeletal muscle clock in response to cancer, that reprograms circadian patterns of gene expression at cachexia onset. Specifically, we show that cancer-induced FoxP1 rewires the skeletal muscle circadian transcriptome towards pathways associated with muscle wasting and disrupts the temporal patterning of pathways governing glucose, lipid, and oxidative metabolism. These findings thus implicate cancer/disease-specific functions of FOXP1 in the disruption and reprograming of the skeletal muscle circadian transcriptome which may contribute to muscle wasting and the development of cachexia.
2025-05-11 | GSE273879 | GEO
Project description:Cachexia is a systemic metabolic syndrome characterized by loss of fat and skeletal muscle mass in chronic wasting diseases such as cancer. The regulation of cellular protein synthesis in response to workload in skeletal muscle is generally blunted in cancer cachexia; however, the precise molecular regulation is largely unknown. In this study, to examine the molecular mechanism of skeletal muscle protein metabolism in cancer cachexia, we analyzed comprehensive gene expression in skeletal muscle using microarrays. CD2F1 mice (male, 7 weeks old) were subcutaneously transplanted (1*10^6 cells per mouse) with a mouse colon cancer-derived cell line (C26) as a model of cancer cachexia. Functional overload of the plantaris muscle by synergist ablation was performed at the 2nd week, and the plantaris muscle was sampled at the 4th week of cancer transplantation. The hypertrophy of skeletal muscle (increased skeletal muscle weight/protein synthesis efficiency and activation of mTOR signaling) associated with compensatory overload was significantly suppressed with the cancer cachexia. Gene expression profiling and pathway analysis by microarray showed that resistance to muscle protein synthesis associated with cancer cachexia was induced by downregulation of insulin-like growth factor-1. These observations show that cancer cachexia induces resistance to muscle protein synthesis, which could be a potential factor inhibiting the adaptation of skeletal muscle growth to physical exercise.
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Project description:Cancer cachexia is a debilitating metabolic disorder characterized by involuntary loss of body and muscle mass, leading to increased morbidity and mortality. We previously found that Forkhead box P1 (FoxP1) upregulation in skeletal muscle causes muscle wasting and is required for muscle wasting in response to cancer. However, transcriptional networks targeted by FoxP1 in skeletal muscles undergoing cancer-induced wasting remain largely unknown. Here, we identify FoxP1 as a key disruptor of the skeletal muscle clock in response to cancer, that reprograms circadian patterns of gene expression at cachexia onset. Specifically, we show that cancer-induced FoxP1 rewires the skeletal muscle circadian transcriptome towards pathways associated with muscle wasting and disrupts the temporal patterning of pathways governing glucose, lipid, and oxidative metabolism. These findings thus implicate cancer/disease-specific functions of FOXP1 in the disruption and reprograming of the skeletal muscle circadian transcriptome which may contribute to muscle wasting and the development of cachexia.
2025-05-11 | GSE273712 | GEO
Project description:Cancer cachexia is a multifactorial wasting syndrome affecting body and lean tissue mass that is often exacerbated by anticancer chemotherapy. In this study, we used a mouse model of acute myeloid leukemia chemotherapy induction regimen (CIR) comprising daunorubicin and cytarabine to investigate the molecular mechanisms underlying cachexia. Quantitative tandem mass tag (TMT) based proteomics was performed on skeletal muscle (quadriceps) to uncover biomarkers and pathways associated with chemotherapy induced muscle wasting. Our findings demonstrate that the AML CIR induced an acute cachexic phenotype characterized by approximately 10 percent body and lean mass loss and 20 percent muscle fibre atrophy. Through deep proteome profiling, two potential biomarkers—haptoglobin (Hp) and glutamine synthetase (Glul)—were identified. Haptoglobin in particular was responsive to cachexia severity, recovery, and exacerbation via exercise, indicating its potential as a conditionally sensitive biomarker of muscle wasting. Pathway analysis revealed upregulation of mitochondrial metabolism including branched chain amino acid catabolism and mitochondrial uncoupling proteins (Ucp1 and Ucp3), suggesting hypermetabolism as a key driver of the phenotype. These data support the use of skeletal muscle proteomics in characterizing chemotherapy induced cachexia and identifying sensitive muscle specific biomarkers for future translational and therapeutic studies.
2025-06-16 | PXD063910 | Pride
Project description:Cancer cachexia is a debilitating metabolic disorder characterized by involuntary loss of body and muscle mass, leading to increased morbidity and mortality. We previously found that Forkhead box P1 (FoxP1) upregulation in skeletal muscle causes muscle wasting and is required for muscle wasting in response to cancer. However, transcriptional networks targeted by FoxP1 in skeletal muscles undergoing cancer-induced wasting remain largely unknown. Here, we identify FoxP1 as a key disruptor of the skeletal muscle clock in response to cancer, that reprograms circadian patterns of gene expression at cachexia onset. Specifically, we show that cancer-induced FoxP1 rewires the skeletal muscle circadian transcriptome towards pathways associated with muscle wasting and disrupts the temporal patterning of pathways governing glucose, lipid, and oxidative metabolism. These findings thus implicate cancer/disease-specific functions of FOXP1 in the disruption and reprograming of the skeletal muscle circadian transcriptome which may contribute to muscle wasting and the development of cachexia.
2025-05-11 | GSE273878 | GEO
Project description:More than 85% of patients with pancreatic ductal adenocarcinoma (PDAC) suffer from cachexia, a debilitating syndrome characterized by loss of muscle and fat. To model PDAC cachexia in mice, 12-week-old C57BL/6J male mice were implanted with the cachexia inducing pancreatic cell line, KPC32908, into the pancreas. Controls underwent a sham surgery. Mice were euthanized under isoflurane anesthesia when the tumor-bearing mice exhibited cachexia, including ~18% loss of quadriceps mass versus sham controls. Quadriceps muscle was flash frozen at euthanasia. 1mg quadriceps protein lysate per sample was used for kinome profiling.
2025-04-21 | PXD047411 | Pride