ArticleScientific reports2024
The autophagy inhibitor NSC185058 suppresses mTORC1-mediated protein anabolism in cultured skeletal muscle.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Autophagy modulation in cancer.Nature reviews. Drug discovery · 2026Review
- MicroRNA-15a/16 regulate protein metabolism and are associated with clinical outcomes in pancreatic ductal adenocarcinoma.Physiological reports · 2026Article
- ATG4B is required for mTORC1-mediated anabolic activity and is associated with clinical outcomes in non-small cell lung cancer.FEBS open bio · 2026Article
- Shaping Cell Identity: Global Transcriptome and Pathway Shifts during Mouse Mammary Epithelial Cell Differentiation.Computational and structural biotechnology journal · 2026Article
- The Influence of Sirtuin 6 on Chondrocyte Senescence in Osteoarthritis Under Aging: Focusing on Mitochondrial Dysfunction and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2025Review
- An overview of autophagy inhibition as a potential clinical strategy in cancer therapy.Molecular pharmacology · 2025Review
- Global mitophagy inhibition via BNIP3 ablation is not sufficient to alleviate skeletal muscle impairments in male and female tumor-bearing mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Article
- Autophagy as a potential therapeutic target in regulating improper cellular proliferation.Frontiers in pharmacology · 2025Review
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9 authors.
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Abstract
The mammalian target of rapamycin (mTOR), and specifically the mTOR complex 1 (mTORC1) is the central regulator of anabolism in skeletal muscle. Among the many functions of this kinase complex is the inhibition of the catabolic process of autophagy; however, less work has been done in investigating the role of autophagy in regulating mTORC1 signaling. Using an in vitro model to better understand the pathways involved, we activated mTORC1 by several different means (growth factors, leucine supplementation, or muscle contraction), alone or with the autophagy inhibitor NSC185058. We found that inhibiting autophagy with NSC185058 suppresses mTORC1 activity, preventing any increase in cellular protein anabolism. These decrements were the direct result of action on the mTORC1 kinase, which we demonstrate, for the first time, cannot function when autophagy is inhibited by NSC185058. Our results indicate that, far from being a matter of unidirectional action, the relationship between mTORC1 and the autophagic cascade is more nuanced, with autophagy serving as an mTORC1 input, and mTORC1 inhibition of autophagy as a form of homeostatic feedback to regulate anabolic signaling. Future studies of cellular metabolism will have to consider this fundamental intertwining of protein anabolism and catabolism, and how it ultimately serves to regulate muscle proteostasis.
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