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Cancer cell-secreted spermidine synthase induces skeletal muscle fibrosis upon radiotherapy (Gastrocnemius muscle)

ABSTRACT: Cancer cell-secreted spermidine synthase induces skeletal muscle fibrosis upon radiotherapy (Gastrocnemius muscle)

PROVIDER: PRJNA1097658 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28591650_1.fastq.gz	Fastqsanger.gz
	SRR28591650_2.fastq.gz	Fastqsanger.gz
	SRR28591651_1.fastq.gz	Fastqsanger.gz
	SRR28591651_2.fastq.gz	Fastqsanger.gz
	SRR28591652_1.fastq.gz	Fastqsanger.gz

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Cancer cell-secreted spermidine synthase induces skeletal muscle fibrosis upon radiotherapy (Gastrocnemius muscle)

Project description:Radiotherapy (RT) reduces the risk of cancer recurrence and death, while accompanied by multiple side effects including muscle fibrosis and weakness, seriously affects the life quality of patients. However, the underlying mechanism is poorly defined. Here, we identify cancer cells secrete more spermidine synthase (SRM) enzyme through small extracellular vesicles (sEVs) to trigger skeletal muscle weakness upon RT. Mechanistically, RT-triggered arachidonic acid (ArA) accumulation elevates the ISGylation of SRM protein, facilitating SRM packaging into EVs from primary tumor. Circulating SRM results in spermidine accumulation in skeletal muscle and type I collagen fiber biosynthesis in an eIF5A-dependent manner. However, losartan treatment blocks the ISGylation of SRM and its subsequent secretion. Collectively, our findings determine that ArA functions in concert for circulating SRM secretion upon RT, which aggravates skeletal muscle fibrosis through rewiring polyamine metabolism, shedding light on the alleviation of RT-mediated muscle weakness when combined with losartan treatment.

2025-04-03 | GSE263507 | GEO

Cancer cell-secreted spermidine synthase induces skeletal muscle fibrosis upon radiotherapy (Gastrocnemius muscle KD)

2025-04-03 | GSE263508 | GEO

Cancer cell-secreted spermidine synthase induces skeletal muscle fibrosis upon radiotherapy (Gastrocnemius muscle KD)

Project description:Cancer cell-secreted spermidine synthase induces skeletal muscle fibrosis upon radiotherapy (Gastrocnemius muscle KD)

| PRJNA1097657 | ENA

Cancer cell-secreted spermidine synthase induces skeletal muscle fibrosis upon radiotherapy (Xenograft tumor)

2025-04-03 | GSE263506 | GEO

Cancer cell-secreted spermidine synthase induces skeletal muscle fibrosis upon radiotherapy (MDA-MB-231)

2025-04-03 | GSE263505 | GEO

Cancer cell-secreted spermidine synthase induces skeletal muscle fibrosis upon radiotherapy (Xenograft tumor)

Project description:Cancer cell-secreted spermidine synthase induces skeletal muscle fibrosis upon radiotherapy (Xenograft tumor)

| PRJNA1097659 | ENA

Cancer cell-secreted spermidine synthase induces skeletal muscle fibrosis upon radiotherapy (MDA-MB-231)

Project description:Cancer cell-secreted spermidine synthase induces skeletal muscle fibrosis upon radiotherapy (MDA-MB-231)

| PRJNA1097655 | ENA

Arachidonic acid triggers spermidine synthase secretion from primary tumor to induce skeletal muscle weakness upon irradiation

Project description:Radiotherapy (RT) reduces the risk of cancer recurrence and death, while accompanied by multiple side effects including muscle weakness, seriously affects the life quality of patients. However, the underlying mechanism is not well defined. Here, we identify cancer cells secrete more spermidine synthase (SRM) protein through small extracellular vesicles (sEVs) to trigger skeletal muscle weakness upon RT. Mechanistically, RT-triggered arachidonic acid (ArA) accumulation elevates the ISGylation of SRM protein, facilitating SRM package into EVs from primary tumor. Circulating SRM proteins enhance spermidine accumulation in skeletal muscle and type I collagen fibers biosynthesis in an eIF5A-dependent manner. Deposition of randomly aligned collogen fibers induced by SRM+ EVs results in skeletal muscle fibrosis and weakness, as well as bone matrix loss. However, losartan treatment blocks the ISGylation of SRM and its subsequent secretion. Collectively, our findings determine that ArA functions in concert for circulating SRM secretion upon RT, which aggravates skeletal muscle fibrosis through rewiring polyamine metabolism, shedding light on the alleviation of RT-mediated muscle weakness when combined with losartan treatment.

2025-04-03 | GSE285652 | GEO

Gastrocnemius muscle-Deletion of TECRL promotes skeletal muscle repair

Project description:Gastrocnemius muscle-Deletion of TECRL promotes skeletal muscle repair

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Matrisome age-related changes in the mouse gastrocnemius muscle

Project description:In recent years, thanks to the great development of mass spectrometry (MS)-based high-throughput proteomic techniques, a large-scale protein characterization is less challenging. Proteomic approaches have been successfully applied to SM in different experimental models [21–24]; however, to date, there is little information on ECM proteins and how they change during ageing. The identification and quantification of ECM components and their interactions are es-sential steps to understand the role of the matrisome in sarcopenia. In this context, we combined a proteomic approach (i.e., LC-MS/MS and bioinformatic analyses) with mor-phological and morphometrical evaluations at fluorescence and transmission electron microscopy of the gastrocnemius muscle in adult and old mice. This age range has been selected since it has been observed that most of changes in muscle protein expression take place after middle age. The gastrocnemius muscle was selected for analysis since it is prevalently composed of fast-twitch fibre, which are especially affected by atrophy during aging. Our findings highlighted several modifications of ECM protein composition and organization in old mice, which likely play a role in the alteration of muscle properties during aging.

2022-02-17 | PXD027895 | Pride

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