RNA Sequencing of TA Muscles from Various Mouse Models of Cachexia
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE227486 | GEO | 2025/03/01
REPOSITORIES: GEO
Similar Datasets
Project description:RNA Sequencing of TA Muscles from Various Mouse Models of Cachexia
| PRJNA945371 | ENA
Project description:Experment1: To study the difference between the parental KPC line and the KPCML1 metastatic cell line Experiment2: 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
2024-04-10 | GSE251864 | GEO
Project description:Cachexia is a systemic wasting syndrome that develops in many cancers and increases mortality. Despite its importance, it is largely unknown how cachexia progressively and differentially induces tissue wasting. Although cachexia occurs also in pediatric patients, little is known on the underlying mechanisms. Here, we have used pediatric melanoma xenografts to determine the progression and tissue-specific impact of juvenile cachexia on skeletal muscles, heart, white and brown adipose, liver, and brain. We find that the heart and muscles undergo wasting at early stages and are the tissues most strongly impacted transcriptionally. Beyond wasting, we identify general and organ-specific transcriptional changes that likely indicate derangement of organ/tissue function by cachexia. Moreover, also the transcriptome of tissues that do not undergo wasting, such as the brain, is profoundly remodeled by cachexia. Altogether, this study provides insight into the progression of melanoma-induced pediatric cachexia and its differential impact on distinct organ systems.
2022-12-15 | GSE183834 | GEO
Project description:Cachexia is a devastating muscle wasting syndrome that occurs in patients suffering from chronic diseases, most commonly observed in 80% of advanced cancer patients. One of the primary causes of cachexia-associated morbidity and mortality is involuntary muscle wasting. And while many cachexia patients show hypermetabolism, its causative role in muscles had remained unclear. To understand the molecular basis of this muscle wasting, accurate models of cachexia are necessary. Using transcriptomics and cytokine profiling of human muscle stem cell-based models and human cancer-induced cachexia models in mice, we found that cachectic cancer cells secreted many inflammatory factors which rapidly led to higher levels of fatty acid metabolism and the activation of a p38 stress response signature, before the cachectic muscle wasting is manifested. Metabolomics profiling revealed that factors secreted by cachectic cancer cells rapidly induce excessive fatty acid oxidation in human myotubes, leading to oxidative stress, p38 activation, and impaired muscle growth. Pharmacological blockade of fatty acid oxidation not only rescued human myotubes, but also significantly improved muscle mass and total weight in cancer cachexia models in vivo. Therefore, fatty acid-induced oxidative stress could be targeted to prevent cancer cachexia.
2016-05-01 | GSE80081 | GEO
Project description:Identification of a Cancer Cachexia Signature through Transcriptomic Analysis of Muscle and Hypothalamic Tissues from CT-26-Induced Cachectic and Control Mice.
2024-11-19 | GSE281701 | GEO
Project description:Cachexia is a wasting syndrome characterized by pronounced skeletal muscle loss. In cancer, cachexia associates with increased morbidity and mortality and decreased treatment tolerance. Although advances have been made in understanding the mechanisms of cachexia, translating these advances to the clinic has been challenging. One reason for this shortcoming may be the current animal models that fail to fully recapitulate the etiology of human cancer-induced tissue wasting. Because pancreatic ductal adenocarcinoma (PDA) presents with a high incidence of cachexia, we engineered a mouse model of PDA, that we named KPP. KPP mice, similar to PDA patients, progressively lose skeletal and adipose mass as a consequence of their tumors. In addition, KPP muscles exhibit a similar gene ontology to cachectic patients. We envision the KPP model will be a useful resource for advancing our mechanistic understanding and ability to treat cancer cachexia.
2019-08-06 | GSE133524 | GEO
Project description:Cachexia is a wasting syndrome characterized by pronounced skeletal muscle loss. In cancer, cachexia associates with increased morbidity and mortality and decreased treatment tolerance. Although advances have been made in understanding the mechanisms of cachexia, translating these advances to the clinic has been challenging. One reason for this shortcoming may be the current animal models that fail to fully recapitulate the etiology of human cancer-induced tissue wasting. Because pancreatic ductal adenocarcinoma (PDA) presents with a high incidence of cachexia, we engineered a mouse model of PDA, that we named KPP. KPP mice, similar to PDA patients, progressively lose skeletal and adipose mass as a consequence of their tumors. In addition, KPP muscles exhibit a similar gene ontology to cachectic patients. We envision the KPP model will be a useful resource for advancing our mechanistic understanding and ability to treat cancer cachexia.
2019-08-06 | GSE133523 | GEO
Project description:RNA sequencing analysis of muscles comparing normal muscles with cachectic muscles isolated from mice bearing distant metastasis from C26m2 and 4T1 murine colon and breast cancer cell lines, collected at the onset of weight loss five weeks after tumor cell injection in these mice.
2018-07-01 | GSE112204 | GEO
Project description:Cancer cachexia is a disorder characterized by both involuntary weight loss and impaired physical performance. Decline in physical performance of patients with cachexia is associated with poor quality of life, and currently there are no effective pharmacological interventions that restore physical performance. Here we examined the effect of GDF15 neutralization in a mouse model of cancer-induced cachexia (TOV21G) that manifested weight loss and muscle function impairments. With comprehensive assessments, our results demonstrated that cachectic mice treated with the anti-GDF15 antibody mAB2 exhibited body weight gain with near-complete restoration of muscle mass and markedly improved muscle function and physical performance. Mechanistically, the improvements induced by GDF15 neutralization were primarily attributed to increased caloric intake, while altered gene expressions in cachectic muscles were restored in both caloric intake-dependent and -independent manners. The findings implicate the potential of GDF15 neutralization as an effective therapy to enhance physical performance of patients with cachexia.
2023-01-11 | GSE214603 | 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