Proteomics analysis of C2C12 myotubes treated with atrophy inducing cancer cell-derived factors.
C26 colon carcinoma
C2C12 myotubes
cancer-associated cachexia
impaired myogenesis
muscle atrophy
Journal
Proteomics
ISSN: 1615-9861
Titre abrégé: Proteomics
Pays: Germany
ID NLM: 101092707
Informations de publication
Date de publication:
26 Oct 2023
26 Oct 2023
Historique:
revised:
12
10
2023
received:
22
06
2023
accepted:
16
10
2023
medline:
26
10
2023
pubmed:
26
10
2023
entrez:
26
10
2023
Statut:
aheadofprint
Résumé
Cancer-associated cachexia is a wasting syndrome that results in dramatic loss of whole-body weight, predominantly due to loss of skeletal muscle mass. It has been established that cachexia inducing cancer cells secrete proteins and extracellular vesicles (EVs) that can induce muscle atrophy. Though several studies examined these cancer-cell derived factors, targeting some of these components have shown little or no clinical benefit. To develop new therapies, understanding of the dysregulated proteins and signaling pathways that regulate catabolic gene expression during muscle wasting is essential. Here, we sought to examine the effect of conditioned media (CM) that contain secreted factors and EVs from cachexia inducing C26 colon cancer cells on C2C12 myotubes using mass spectrometry-based label-free quantitative proteomics. We identified significant changes in the protein profile of C2C12 cells upon exposure to C26-derived CM. Functional enrichment analysis revealed enrichment of proteins associated with inflammation, mitochondrial dysfunction, muscle catabolism, ROS production, and ER stress in CM treated myotubes. Furthermore, strong downregulation in muscle structural integrity and development and/or regenerative pathways were observed. Together, these enriched proteins in atrophied muscle could be utilized as potential muscle wasting markers and the dysregulated biological processes could be employed for therapeutic benefit in cancer-induced muscle wasting.
Identifiants
pubmed: 37882347
doi: 10.1002/pmic.202300020
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e2300020Subventions
Organisme : Australian Research Council Future Fellowship
ID : FT180100333
Informations de copyright
© 2023 The Authors. Proteomics published by Wiley-VCH GmbH.
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