ArticleJournal of translational medicine2022
Heme oxygenase 1 overexpression induces immune evasion of acute myeloid leukemia against natural killer cells by inhibiting CD48.
Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- A single-cell atlas of peripheral immunity suggests immune subset attrition during tuberculosis dissemination.The Journal of international medical research · 2026Article
- Lipid metabolism and chromatin-associated sirtuin-dependent epigenetic reprogramming in cancer.Molecular biology reports · 2026Review
- Genome-wide investigation of differentially expressed alternative splicing and RNA-binding protein genes association with AML drug resistance.Discover oncology · 2026Article
- HO-1-driven drug resistance in hematological malignancies: Mechanistic insights and advances in targeted therapy.iScience · 2026Review
- Dual Regulatory Functions and Therapeutic Potential of CD48 in Tumor Immunity.Oncology research · 2026Review
- SLAMF receptors: key regulators of tumor progression and emerging targets for cancer immunotherapy.Molecular cancer · 2025Review
- Heme oxygenase 1 confers gilteritinib resistance in FLT3-ITD acute myeloid leukemia in a STAT6-dependent manner.Cancer cell international · 2025Article
- Bone marrow immune cells and drug resistance in acute myeloid leukemia.Experimental biology and medicine (Maywood, N.J.) · 2025Review
- Harnessing peroxisome proliferator-activated receptor γ agonists to induce Heme Oxygenase-1: a promising approach for pulmonary inflammatory disorders.Cell communication and signaling : CCS · 2024Review
- The role of exhausted natural killer cells in the immunopathogenesis and treatment of leukemia.Cell communication and signaling : CCS · 2024Review
- A hypoxia-related genes prognostic risk model, and mechanisms of hypoxia contributing to poor prognosis through immune microenvironment and drug resistance in acute myeloid leukemia.Frontiers in pharmacology · 2024Article
- Heme catabolism and heme oxygenase-1-expressing myeloid cells in pathophysiology.Frontiers in immunology · 2024Review
- The prognostic and therapeutic potential of HO-1 in leukemia and MDS.Cell communication and signaling : CCS · 2023Review
- Unveiling T cell evasion mechanisms to immune checkpoint inhibitors in acute myeloid leukemia.Cancer drug resistance (Alhambra, Calif.) · 2023Review
- The promise of targeting heme and mitochondrial respiration in normalizing tumor microenvironment and potentiating immunotherapy.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute myeloid leukemia (AML) is the most common type of acute leukemia in adults. Given the high relapse rate, more effective treatments are needed to improve clinical outcomes. We previously demonstrated that heme oxygenase 1 (HO1) is overexpressed in AML, while the functional roles of HO1 remain unclear.
methodsBioinformatics analysis and flow cytometry were conducted to assess the association between HO1 levels and immune cells or immune checkpoint/ligand molecules in AML patients. Primary natural killer (NK) cells were purified and subsequently co-cultured in vitro with transduced AML cells to determine the effects of HO1 expression on NK cell functions. AML mice models were established to investigate the effects of HO1 expression on cytotoxic effects of NK cells in vivo. The molecular mechanism was studied by flow cytometry, quantitative real-time PCR (qRT-PCR), western blotting, and immunoprecipitation.
resultsBioinformatics analysis indicated a correlation between HO1 expression and the AML immune microenvironment. The present study findings indicated that HO1 specifically downregulates the expression of CD48, a ligand of the NK cell-activating receptor 2B4, thus decreasing the cytotoxic effect of NK cells. HO1 overexpression promoted tumor growth and inhibited the cytotoxic effect of NK cells in the AML mice model. Mechanistic investigations found that HO1 directly interacted with Sirt1 and increased its expression and deacetylase activity. With the overexpression of HO1, increased Sirt1 in AML cells enabled histone H3K27 deacetylation to suppress CD48 transcription and expression. Administration of Sirt1 inhibitor restored the expression of CD48.
conclusionsCollectively, HO1 promotes NK cell dysfunction in AML. Therefore, restoring NK cell function by inhibiting HO1 activity is a potential immunotherapeutic approach against AML.
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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 Socratic graph.