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

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

PROVIDER: PRJNA615799 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11431709.fastq.gz	Fastqsanger.gz
	SRR11431710.fastq.gz	Fastqsanger.gz
	SRR11431711.fastq.gz	Fastqsanger.gz
	SRR11431712.fastq.gz	Fastqsanger.gz
	SRR11431713.fastq.gz	Fastqsanger.gz

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

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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.

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Blocking muscle wasting via deletion of the muscle specific E3 ligase MuRF1 impedes pancreatic tumor growth - proteome dataset

Project description:Cancer-induced muscle wasting reduces quality of life, complicates or precludes cancer treatments, and predicts early mortality. Herein, we investigated the requirement of the muscle-specific E3 ubiquitin ligase, MuRF1, for muscle wasting induced by pancreatic cancer. Murine pancreatic cancer (KPC) cells, or saline, were injected into the pancreas of WT and MuRF1-/- mice, and tissues analyzed throughout tumor progression. KPC tumors induced progressive wasting of skeletal muscle and systemic metabolic reprogramming in WT mice, but not MuRF1-/- mice. KPC tumors from MuRF1-/- mice also grew slower, and showed an accumulation of metabolites normally depleted by rapidly growing tumors. Mechanistically, MuRF1 was necessary for the KPC-induced increases in cytoskeletal and muscle contractile protein ubiquitination, and the depression of proteins that support protein synthesis. Together, these data demonstrate that MuRF1 is required for KPC-induced skeletal muscle wasting, whose deletion reprograms the systemic and tumor metabolome and delays tumor growth.

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Blocking muscle wasting via deletion of the muscle specific E3 ligase MuRF1 impedes pancreatic tumor growth – ubiquitome dataset

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Systemic muscle wasting drives tumourigenesis

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Project description:Reduced PABPN1 levels cause aging-associated muscle wasting. PABPN1 is a multi-functional regulator of mRNA processing. To elucidate the molecular mechanisms causing PABPN1-mediated muscle wasting, we compared the transcriptome to the proteome in mouse muscles expressing shRNA to PABPN1 (shPab). We found greater variations in the proteome as compared to mRNA expression profiles. Protein accumulation in the shPab proteome was concomitant with reduced proteasomal activity. Notably, protein acetylation appeared to be enriched in shPab versus control proteomes (63%). An acetylome study in shPab muscles revealed prominent peptide deacetylation associated with elevated sirtuin-1 (SIRT1) deacetylase. We show that SIRT1 mRNA levels are controlled by PABPN1 via an alternative polyadenylation site utilization. SIRT1 inhibition reversed PABPN1 activity and muscle cell function. Moreover, deacetylation inhibition increased PABPN1 levels and reversed muscle wasting. We suggest that perturbation of a multifactorial regulatory loop involving PABPN1 and SIRT1 plays an imperative role in aging-associated muscle wasting.

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