ArticleJournal of translational medicine2025
Vorinostat impairs the cancer-driving potential of leukemia-secreted extracellular vesicles.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Optimizing pyrazine-2-carboxamide derivatives as dual FLT3/HDAC inhibitors with enhanced pharmacokinetics and immunotherapeutic potential.Acta pharmaceutica Sinica. B · 2026Article
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Authors and funding
14 authors.
Funding
Abstract
backgroundLeukemia-secreted extracellular vesicles (EVs) carry biologically active cargo that promotes cancer-supportive mechanisms, including aberrant proliferative signaling, immune escape, and drug resistance. However, how antineoplastic drugs affect EV secretion and cargo sorting remains underexplored.
methodsLeukemia-secreted extracellular vesicles (EVs) were isolated by Differential UltraCentrifugation, and their miRNome and proteomic profiling cargo were analyzed following treatment with SAHA (Vorinostat) in Acute Myeloid Leukemia (AML) and Chronic Myeloid Leukemia (CML). The epigenetic modulation of leukemia-secreted EVs content on interesting key target molecules was validated, and their differential functional impact on cellular viability, cell cycle progression, apoptosis, and tumorigenicity was assessed.
resultsSAHA significantly alters the cargo of Leukemia-derived EVs, including miR-194-5p and its target BCLAF1 (mRNA and protein), key regulators of Leukemia cell survival and differentiation. SAHA upregulates miR-194-5p expression while selective loading BCLAF1 into EVs, reducing the miRNA levels in the same compartment. Additionally, SAHA alters miRNA profile and proteomic composition associated with leukemic EVs, altering their tumor-supportive potential, with differential effects observed between AML and CML. Furthermore, in silico predictions suggest that these modified EVs may influence cell sensitivity to antineoplastic agents, suggesting a dual role for SAHA in impairing oncogenic signaling while enhancing therapeutic responsiveness.
conclusionsIn conclusion, the capacity of SAHA to modulate secretion and molecular composition of Leukemia-secreted EVs, alongside its direct cytotoxic effects, underscores its potential in combination therapies aimed to overcoming refractory phenotype by targeting EV-mediated communication.
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