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Highly effective combination of LSD1 (KDM1A) antagonist and pan-histone deacetylase inhibitor against human AML cells
Open accessAbstract
The histone demethylase LSD1 (KDM1A) demethylates mono- and di-methylated (Me2) lysine (K) 4 on histone H3. High LSD1 expression blocks differentiation and confers a poor prognosis in acute myeloid leukemia (AML). Here, treatment with the novel LSD1 antagonist SP2509 attenuated the binding of LSD1 with the corepressor CoREST, increased the permissive H3K4Me3 mark on the target gene promoters, and increased the levels of p21, p27 and CCAAT/enhancer binding protein α in cultured AML cells. In addition, SP2509 treatment or LSD1 shRNA inhibited the colony growth of AML cells. SP2509 also induced morphological features of differentiation in the cultured and primary AML blasts. SP2509 induced more apoptosis of AML cells expressing mutant NPM1 than mixed-lineage leukemia fusion oncoproteins. Treatment with SP2509 alone significantly improved the survival of immune-depleted mice following tail-vein infusion and engraftment of cultured or primary human AML cells. Co-treatment with pan-HDAC inhibitor (HDI) panobinostat (PS) and SP2509 was synergistically lethal against cultured and primary AML blasts. Compared with each agent alone, co-treatment with SP2509 and PS significantly improved the survival of the mice engrafted with the human AML cells, without exhibiting any toxicity. Collectively, these findings show that the combination of LSD1 antagonist and pan-HDI is a promising therapy warranting further testing against AML.
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“These findings support and provide a molecular explanation for recent observations that combination therapies of KDM1A antagonist and HDAC inhibitors exhibit an enhanced response29.”
From Efficient combinatorial targeting of RNA transcripts in single cells with Cas13 RNA Perturb-seq (2023) · cites this paper as [29]
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Metadata
- Authors
- Fiskus, W., Sharma, S., Shah, B., Portier, B. P., Devaraj, S. G. T., Liu, K., Iyer, S. P., Bearss, D., & Bhalla, K. N.
- Affiliations
- Houston Methodist (US)
- University of Utah (US)
- Brigham Young University (US)
- Corresponding author
- Bhalla, K N
- Venue
- Leukemia
- Published
- 2014-04-04
- Volume
- 28
- Issue
- 11
- Pages
- 2155-2164
- ISSN
- 0887-6924 (ISSN-L)
- 1476-5551
- PMC
- PMC4739780
- OpenAlex
- W2006229882
- Cited by
- 284
- References
- 45
- Citations by year
- 2026: 8 · 2025: 14 · 2024: 21 · 2023: 18 · 2022: 20 · 2021: 18 · 2020: 25 · 2019: 27 · 2018: 26 · 2017: 45 · 2016: 35 · 2015: 21 · 2014: 5
- FWCI
- 25.06
- Type
- journal article
- Language
- en
- Update notices
- erratum (2017-03-21)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Leukemia (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R01CA171338, R01CA173877, R01CA123207)
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Keywords
- LSD1, acute myeloid leukemia, histone deacetylase inhibitors, panobinostat, combination therapy, H3K4 demethylation, leukemia cell differentiation, apoptosis, NPM1 mutation, MLL fusion, synergistic lethality
- MeSH terms
- Nucleophosmin, Animals, Cells, Cultured, Disease Models, Animal, Enzyme Inhibitors, Female, Histones, Humans, Hydrazines, Nerve Tissue Proteins, Stem Cells, Sulfonamides, Tumor Cells, Cultured, Leukemia, Myeloid, Acute, Mice, SCID, Mice, Inbred NOD, Apoptosis, Xenograft Model Antitumor Assays, RNA, Small Interfering, Histone Acetyltransferases, Histone Demethylases, Co-Repressor Proteins
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