ArticleMolecular & cellular proteomics : MCP2019
Cathepsin L Regulates Metabolic Networks Controlling Rapid Cell Growth and Proliferation.
Article in Molecular & cellular proteomics : MCP, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
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- Targeting Glycolysis with 2-Deoxy-D-Glucose and Lysosomal Integrity with L-Leucyl-L-Leucine Methyl Ester as Antimelanoma Strategy.Pharmaceutics · 2025Article
- Exploring the role of Cathepsin S in mitochondrial energy metabolism: implications for cancer progression and therapeutic targeting.Medical oncology (Northwood, London, England) · 2025Review
- Construction of a Core Germplasm and Identification of Candidate SNPs Associated with Growth Performance of Epinephelus tukula by Whole-Genome Resequencing.Marine biotechnology (New York, N.Y.) · 2025Article
- Cathepsins: Emerging targets in the tumor ecosystem to overcome cancers.Seminars in cancer biology · 2025Review
- Morphotype-Specific Antifungal Defense inInsects · 2025Article
- Novel Nucleus-Oriented Quenched Activity-Based Probes Link Cathepsin Nuclear Localization with Mitosis.ACS sensors · 2025Article
- Associations of cathepsins with pulmonary arterial hypertension mediated by circulating metabolites: A Mendelian randomization study.Medicine · 2025Article
- Immunostimulant Bathing Influences the Expression of Immune- and Metabolic-Related Genes in Atlantic Salmon Alevins.Biology · 2021Article
- Cathepsin Inhibition Modulates Metabolism and Polarization of Tumor-Associated Macrophages.Cancers · 2020Article
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rapidly proliferating cells reshape their metabolism to satisfy their ever-lasting need for cellular building blocks. This phenomenon is exemplified in certain malignant conditions such as cancer but also during embryonic development when cells rely heavily on glycolytic metabolism to exploit its metabolic intermediates for biosynthetic processes. How cells reshape their metabolism is not fully understood. Here we report that loss of cathepsin L (Cts L) is associated with a fast proliferation rate and enhanced glycolytic metabolism that depend on lactate dehydrogenase A (LDHA) activity. Using mass spectrometry analysis of cells treated with a pan cathepsin inhibitor, we observed an increased abundance of proteins involved in central carbon metabolism. Further inspection of putative Cts L targets revealed an enrichment for glycolytic metabolism that was independently confirmed by metabolomic and biochemical analyses. Moreover, proteomic analysis of Cts L-knockout cells identified LDHA overexpression that was demonstrated to be a key metabolic junction in these cells. Lastly, we show that Cts L inhibition led to increased LDHA protein expression, suggesting a causal relationship between LDHA expression and function. In conclusion, we propose that Cts L regulates this metabolic circuit to keep cell division under control, suggesting the therapeutic potential of targeting this protein and its networks in cancer.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.