ArticleMedical oncology (Northwood, London, England)2023
Dexamethasone enhances venetoclax-induced apoptosis in acute myeloid leukemia cells.
Article in Medical oncology (Northwood, London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Mitochondrial DNA mutations and intercellular mitochondrial transfer in cancer: mechanisms, biological effects, and clinical potential.Biomarker research · 2026Review
- Comparative Analysis of the Therapeutic Efficacy of Decitabine Combined with Cytarabine, Aclarubicin, and Granulocyte Colony-stimulating Factor (D-CAG) Versus CAG Regimen in the Treatment of Acute Myeloid Leukemia.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2025Article
- Targeting METTL3 mitigates venetoclax resistance via proteasome-mediated modulation of MCL1 in acute myeloid leukemia.Cell death & disease · 2025Article
- Potential value of immunogenic cell death related-genes in refining European leukemiaNet guidelines classification and predicting the immune infiltration landscape in acute myeloid leukemia.Cancer cell international · 2025Article
- Recent advancements in biomarkers, therapeutics, and associated challenges in acute myeloid leukemia.Annals of hematology · 2024Review
- NET-related gene signature for predicting AML prognosis.Scientific reports · 2024Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Acute myeloid leukemia (AML) therapies have been significantly improved by the development of medicines that can target BCL-2. On the other hand, non-recurrent alterations in oncogenic pathways and gene expression patterns have already been linked to therapeutic resistance to venetoclax therapy. Bone marrow mesenchymal stromal cells (BM-MSCs) support leukemic cells in preventing chemotherapy-induced apoptosis by mitochondrial transfer in leukemic microenvironment. In this study, we investigated the enhancement of the antitumor effect of BCL-2 inhibitor venetoclax by dexamethasone. In particular, dexamethasone had no significant effect on the viability of AML cells, but dexamethasone combined with venetoclax could significantly increase the apoptosis of AML cells induced by venetoclax. When AML cells were co-cultured with BM-MSCs, dexamethasone combined with venetoclax showed additional anti-tumor effect compared to venetoclax alone. Venetoclax increased reactive oxygen species level in co-cultured AML cells, contributed to transfer more mitochondria from BM-MSCs to AML cells and protect AML cells from apoptosis. Dexamethasone combined with venetoclax induced more apoptosis, but dexamethasone reduced the venetoclax-induced reactive oxygen species level in AML cells and reduced the transfer of mitochondria from BM-MSCs to AML cells. This may lead to a diminished protective effect of BM-MSCs on AML cells. Together, our findings indicated that venetoclax in combination with dexamethasone could be a promising therapy in AML.
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