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Paeonia lactiflora suppressed cancer-cachexia by downregulating muscular NF-κB signaling and muscle-specific E3 ubiquitin ligases in cancer-bearing mice.

ABSTRACT: Paeonia lactiflora suppressed cancer-cachexia by downregulating muscular NF-κB signaling and muscle-specific E3 ubiquitin ligases in cancer-bearing mice.

PROVIDER: PRJNA545980 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9188640.fastq.gz	Fastqsanger.gz
	SRR9188641.fastq.gz	Fastqsanger.gz
	SRR9188642.fastq.gz	Fastqsanger.gz
	SRR9188643.fastq.gz	Fastqsanger.gz
	SRR9188644.fastq.gz	Fastqsanger.gz

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Paeonia lactiflora suppressed cancer-cachexia by downregulating muscular NF-κB signaling and muscle-specific E3 ubiquitin ligases in cancer-bearing mice.

Project description:Paeonia lactiflora restored skeletal muscle function and mass in cancer-bearing mice, through the downregulations of muscular NF-kB signalling and muscle-specific E3 ubiquitin ligases. This study provides experimental evidence that Paeonia lactiflora can be a plausible candidate for a therapeutic agent for cancer cachexia.

2019-06-04 | GSE132120 | GEO

Paeonia lactiflora extract suppresses cisplatin-induced muscle wasting via donwnregulations of muscle-specific E3 ubiquitin ligases

Project description:Cisplatin is a broad-spectrum anti-cancer drugs used in diverse types of cancer, however, muscle wasting is one of the most common side effects of cisplatin chemotherapy. This study aimed to elucidate the effects of an ethanol extract of the root of Paeonia lactiflora Pall. (Radix Paeoniae, RP) on cisplatin-induced muscle wasting along with its molecular mechanism.

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Paeonia lactiflora extract suppresses cisplatin-induced muscle wasting via donwnregulations of muscle-specific E3 ubiquitin ligases

Project description:Paeonia lactiflora extract suppresses cisplatin-induced muscle wasting via donwnregulations of muscle-specific E3 ubiquitin ligases

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Modeling Human Cancer-induced Cachexia (Mouse)

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.

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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.

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Project description:Cancer cachexia and the associated skeletal muscle wasting are considered poor prognostic factors, although effective treatment has not yet been established. Recent studies have indicated that the pathogenesis of skeletal muscle loss may involve dysbiosis of the gut microbiota and the accompanying chronic inflammation or altered metabolism. In this study, we evaluated the possible effects of modifying the gut microenvironment with partially hydrolyzed guar gum (PHGG), a soluble dietary fiber, on cancer-related muscle wasting and its mechanism using a colon-26 murine cachexia model. Compared to a fiber-free (FF) diet, PHGG contained fiber-rich (FR) diet attenuated skeletal muscle loss in cachectic mice by suppressing the elevation of the major muscle-specific ubiquitin ligases Atrogin-1 and MuRF1, as well as the autophagy markers LC3 and Bnip3. Although tight junction markers were partially reduced in both FR and FF diet-fed cachectic mice, the abundance of Bifidobacterium, Akkermansia, and unclassified S24-7 family increased by FR diet, contributing to the retention of the colonic mucus layer. The reinforcement of the gut barrier function resulted in the controlled entry of pathogens into the host system and reduced circulating levels of lipopolysaccharide-binding protein (LBP) and IL-6, which in turn led to the suppression of proteolysis by downregulating the ubiquitin-proteasome system and autophagy pathway. These results suggest that dietary fiber may have the potential to alleviate skeletal muscle loss in cancer cachexia, providing new insights for developing effective strategies in the future.

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ADIPOSE TISSUE PATHWAYS INVOLVED IN WEIGHT LOSS OF CANCER CACHEXIA

Project description:The regulatory gene pathways underlying the loss of adipose tissue in cancer cachexia are unknown and were explored using pangenomic transcriptome profiling. Gene expression profiles (Human Gene 1.0 ST) of abdominal subcutaneous adipose tissue were studied in gastrointestinal cancer patients with (N=13) or without (N=14) cachexia. Data analyses were performed using the Affymetrix GeneChip Operating Software (GCOS) Version 1.4.

2010-04-10 | E-GEOD-20571 | biostudies-arrayexpress

Neural invasion induces cachexia via astrocytic activation of neural route in pancreatic cancer

Project description:Pancreatic cancer is characterized by a high frequency of cachexia, pain and neural invasion (N-inv). Neural damage is occurred by N-inv and modulates pain and muscle atrophy via the activation of astrocyte in the connected spine. The activated astrocyte by N-inv, thus, may affect cachexia in pancreatic cancer. Clinical studies in patients and autopsy cases with pancreatic cancer have revealed that N-inv is related to cachexia and astrocytic activation. We established a novel murine model of cancer cachexia using N-inv of human pancreatic cancer cells. Mice with N-inv showed a loss of body weight, skeletal muscle, and fat mass without appetite loss, which are compatible with an animal model of cancer cachexia. Activation of astrocytes in the spinal cord connected with N-inv was observed in our model. Experimental cachexia was suppressed by disrupting neural routes or inhibiting the activation of astrocytes. These data provide the first evidence that N-inv induces cachexia via astrocytic activation of neural route in pancreatic cancer. We produced neural invasion (N-inv) model using intraneural injection of Capan-1 cells to left sciatic nerve of male SCID mouse. For controls, subcutaneous model (SC) and PBS model were produced. Microarray analysis was performed using the first lumbar cord (L1) from PBS, SC, and N-inv mice at 6 w (n = 2 each).

2011-12-07 | E-GEOD-34189 | biostudies-arrayexpress

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