ArticleJournal of immunology (Baltimore, Md. : 1950)2024
The Proteasome Inhibitor Bortezomib Induces p53-Dependent Apoptosis in Activated B Cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2024. 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, 7 citations in OpenAlex.
- Molecular mechanisms underlying liposarcoma subtype transition and proteasome-associated targeted interventions.Journal of translational medicine · 2026Review
- Targeting mutant p53 in cancer: from mechanistic insights to therapeutic strategies.Cellular & molecular biology letters · 2026Review
- Impact of immune cell metabolism on membranous nephropathy and prospective therapy.Communications biology · 2025Review
- The Ubiquitin-Proteasome System: A Key Regulatory Hub in Myocarditis Leading to Dilated Cardiomyopathy.Journal of inflammation research · 2025Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The proteasome inhibitor bortezomib (BTZ) is proposed to deplete activated B cells and plasma cells. However, a complete picture of the mechanisms underlying BTZ-induced apoptosis in B lineage cells remains to be established. In this study, using a direct in vitro approach, we show that deletion of the tumor suppressor and cell cycle regulator p53 rescues recently activated mouse B cells from BTZ-induced apoptosis. Furthermore, BTZ treatment elevated intracellular p53 levels, and p53 deletion constrained apoptosis, as recently stimulated cells first transitioned from the G1 to S phase of the cell cycle. Moreover, combined inhibition of the p53-associated cell cycle regulators and E3 ligases MDM2 and anaphase-promoting complex/cyclosome induced cell death in postdivision B cells. Our results reveal that efficient cell cycle progression of activated B cells requires proteasome-driven inhibition of p53. Consequently, BTZ-mediated interference of proteostasis unleashes a p53-dependent cell cycle-associated death mechanism in recently activated B cells.
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Registered trials
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