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A molecular pathway for cancer cachexia-induced muscle atrophy revealed at single nucleus resolution [Bulk_RNAseq]

ABSTRACT: A molecular pathway for cancer cachexia-induced muscle atrophy revealed at single nucleus resolution [Bulk_RNAseq]

PROVIDER: PRJNA1135087 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29803451.fastq.gz	Fastqsanger.gz
	SRR29803452.fastq.gz	Fastqsanger.gz
	SRR29803453.fastq.gz	Fastqsanger.gz
	SRR29803454.fastq.gz	Fastqsanger.gz
	SRR29803455.fastq.gz	Fastqsanger.gz

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A molecular pathway for cancer cachexia-induced muscle atrophy revealed at single nucleus resolution [Bulk_RNAseq]

Project description:Cancer cachexia is a prevalent and often fatal wasting condition that cannot be fully reversed with nutritional interventions. Muscle atrophy is a central component of the syndrome, but the mechanisms whereby cancer leads to skeletal muscle atrophy are not well understood. We performed single nucleus multi-omics on skeletal muscles from a mouse model of cancer cachexia and profiled the molecular changes in cachexic muscle. Our results revealed the activation of a denervation-induced gene program that upregulates the transcription factor myogenin. Further studies showed that a myogenin-myostatin pathway promotes muscle atrophy in response to cancer cachexia. shRNA inhibition of myogenin or inhibition of myostatin through overexpression of its endogenous inhibitor follistatin prevented cancer cachexia-induced muscle atrophy in mice. Our findings uncover a molecular basis of cancer cachexia-induced muscle atrophy and highlight potential therapeutic targets for this disorder.

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A molecular pathway for cancer cachexia-induced muscle atrophy revealed at single nucleus resolution [scRNA]

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A molecular pathway for cancer cachexia-induced muscle atrophy revealed at single nucleus resolution [snATAC]

Project description:A molecular pathway for cancer cachexia-induced muscle atrophy revealed at single nucleus resolution [snATAC]

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A molecular pathway for cancer cachexia-induced muscle atrophy revealed at single nucleus resolution [scRNA]

Project description:A molecular pathway for cancer cachexia-induced muscle atrophy revealed at single nucleus resolution [scRNA]

| PRJNA1135088 | ENA

Methionine cycle dysregulation mediates REDD1 overexpression-induced muscle atrophy in cancer cachexia

Project description:The essential amino acid methionine plays a pivotal role in one-carbon metabolism, facilitating the production of S-adenosylmethionine (SAMe), a critical supplier for DNA methylation. Here we find the disruption of methionine metabolism by rapid SAMe depletion in skeletal muscle in cancer cachexia, leading to endoplasmic reticulum (ER) stress and the overexpression of regulated in development and DNA damage responses (REDD1). Targeting the DNA methylation process via DNA methyltransferases (DNMTs) and REDD1 knockout can alleviate cancer cachexia-induced skeletal muscle atrophy. Methionine supplementation maintains the DNA methylation of DNA damage-inducible transcript 4 (Ddit4) by DNMT3A, thereby inhibiting activating transcription factor 4 (ATF4)-mediated Ddit4 transcription. Our study suggests that methionine or SAMe supplementation can effectively reverse muscle atrophy in cancer cachexia, providing valuable mechanistic insights and a promising therapeutic strategy for clinical application.

2024-10-11 | GSE275001 | GEO

Leukemia Inhibitory Factor in C26 Cancer Cachexia

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

Excessive fatty acid oxidation induces muscle atrophy in cancer cachexia

Project description:Excessive fatty acid oxidation induces muscle atrophy in cancer cachexia

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Leukemia Inhibitory Factor in C26 Cancer Cachexia

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Epigenetic Targeting of Bromodomain Protein BRD4 Counteracts Cancer Cachexia and Prolongs Survival

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