ArticleCell death & disease2025
Cathepsin D promotes acute myeloid leukemia progression through stabilization of the anti-apoptotic proteins.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Targeting lysosome-dependent cell death in cancer: towards therapeutic strategies.Biomarker research · 2026Review
- Helminth-derived stefin-1 selectively reduces leukemic cell viability and promotes apoptosis in U937 cells.PloS one · 2026Article
- Article
- Asparagine-related biomarkers and regulatory mechanisms in type 2 diabetes mellitus.Frontiers in molecular biosciences · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
Cathepsin D (CTSD) is a lysosomal aspartic protease that plays vital roles in regulating the properties of solid tumors, including proliferation, apoptosis, migration, metastasis, and angiogenesis. However, the function of CTSD in haematological malignancies remains largely elusive. Here we show that CTSD is highly expressed in acute myeloid leukemia (AML) and that high CTSD expression is associated with unfavourable prognosis. Knockdown of CTSD in AML cells inhibits cell proliferation and anti-apoptotic activity. Mechanistically, CTSD decreased the expression of the E3 ubiquitin ligase TRIM21, which mediates the ubiquitination and degradation of anti-apoptotic proteins BCL2, BCL-XL, and MCL1. Inhibition of CTSD expression via genetics or the small-molecule inhibitor N-8 decreases the protein levels of BCL2, BCL-XL, and MCL1 through accelerating their degradation. N-8 shows significant efficacy in eradicating AML in both venetoclax-sensitive and -resistant models. Collectively, our study reveals the role of CTSD in leukemia progression and highlights targeting CTSD as a potential therapeutic strategy in AML.
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