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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.

2020-03-28 | GSE147613 | GEO

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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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).

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Preclinical investigation of the novel histone deacetylase inhibitor AR-42 in the treatment of cancer-induced cachexia

Project description:Purpose: We assessed the anti-cachectic activity of the novel HDAC inhibitor AR-42 in murine models of cancer cachexia. Methods: Effects on classic features of cachexia, including decreased body weight, skeletal muscle and adipose tissue mass, muscle fiber cross-sectional area, and muscle strength, and increased intramuscular mRNA expression of E3 ligases Atrogin-1/MAFbx and MuRF1 were examined. Metabolomic analysis, whole transcriptome shotgun sequencing (RNA-seq) analysis, and cytokine profiling were used to compare metabolic phenotype and mRNA expression profiles in muscle, and cytokine production in serum, respectively, in AR-42- and vehicle-treated tumor-bearing and tumor-free control mice. Results: Orally administered AR-42 suppressed cancer cachexia in the C-26 colon adenocarcinoma model. This anti-cachectic effect, also confirmed in Lewis lung carcinoma-bearing mice, was not observed after treatment with other HDAC inhibitors (vorinostat, romidepsin). Cytokine profiling and RNA-seq analyses revealed effects of AR-42 on tumor-induced changes in inflammatory cytokine production and multiple transcriptional programs in muscle, including the inhibition of multiple pro-cachexia drivers, such as IL-6 and its receptor IL-6ra, leukemia inhibitory factor, Foxo1, Atrogin-1, MuRF1, adipose triglyceride lipase, uncoupling protein 3, and myocyte enhancer factor 2c. Metabolomic analysis indicated the reprogramming of skeletal muscle metabolism, including reduced glycolysis and glycogen synthesis and increased protein degradation, which was restored by AR-42 to a state characteristic of tumor-free mice. Conclusions: These findings support further investigation of AR-42 as part of a comprehensive therapeutic strategy for cancer cachexia.

2015-03-13 | GSE65936 | GEO

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Project description:Paeonia lactiflora Organism overview

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