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Journal articles on the topic 'Complexo LSD1'

Author: Grafiati

Published: 4 September 2021

Last updated: 29 July 2025

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1

Marayati, Bahjat F., James F. Tucker, David A. De La Cerda, et al. "The Catalytic-Dependent and -Independent Roles of Lsd1 and Lsd2 Lysine Demethylases in Heterochromatin Formation in Schizosaccharomyces pombe." Cells 9, no. 4 (2020): 955. http://dx.doi.org/10.3390/cells9040955.

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In eukaryotes, heterochromatin plays a critical role in organismal development and cell fate acquisition, through regulating gene expression. The evolutionarily conserved lysine-specific demethylases, Lsd1 and Lsd2, remove mono- and dimethylation on histone H3, serving complex roles in gene expression. In the fission yeast Schizosaccharomyces pombe, null mutations of Lsd1 and Lsd2 result in either severe growth defects or inviability, while catalytic inactivation causes minimal defects, indicating that Lsd1 and Lsd2 have essential functions beyond their known demethylase activity. Here, we sho

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Liu, Haoran, Bahjat Fadi Marayati, David de la Cerda, et al. "The Cross-Regulation Between Set1, Clr4, and Lsd1/2 in Schizosaccharomyces pombe." PLOS Genetics 20, no. 1 (2024): e1011107. http://dx.doi.org/10.1371/journal.pgen.1011107.

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Eukaryotic chromatin is organized into either silenced heterochromatin or relaxed euchromatin regions, which controls the accessibility of transcriptional machinery and thus regulates gene expression. In fission yeast, Schizosaccharomyces pombe, Set1 is the sole H3K4 methyltransferase and is mainly enriched at the promoters of actively transcribed genes. In contrast, Clr4 methyltransferase initiates H3K9 methylation, which has long been regarded as a hallmark of heterochromatic silencing. Lsd1 and Lsd2 are two highly conserved H3K4 and H3K9 demethylases. As these histone-modifying enzymes perf

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Storck, William K., Vincent T. Bicocca, Michael R. Rountree, Shinji Honda, Tereza Ormsby, and Eric U. Selker. "LSD1 prevents aberrant heterochromatin formation in Neurospora crassa." Nucleic Acids Research 48, no. 18 (2020): 10199–210. http://dx.doi.org/10.1093/nar/gkaa724.

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Abstract Heterochromatin is a specialized form of chromatin that restricts access to DNA and inhibits genetic processes, including transcription and recombination. In Neurospora crassa, constitutive heterochromatin is characterized by trimethylation of lysine 9 on histone H3, hypoacetylation of histones, and DNA methylation. We explored whether the conserved histone demethylase, lysine-specific demethylase 1 (LSD1), regulates heterochromatin in Neurospora, and if so, how. Though LSD1 is implicated in heterochromatin regulation, its function is inconsistent across different systems; orthologs o

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Fiskus, Warren, Christopher Peter Mill, Christine Birdwell, et al. "Pre-Clinical Efficacy of Co-Targeting GFI1/KDM1A and BRD4 or JAK1/2 Against AML and Post-MPN Secondary AML Blast Progenitor Cells." Blood 136, Supplement 1 (2020): 27. http://dx.doi.org/10.1182/blood-2020-140212.

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Transcriptional regulators (TFs) involved in cell-growth, differentiation and survival of AML stem/progenitor cells (LSCs) include RUNX1, PU.1, CEBPα, c-Myb and c-Myc. LSD1 (KDM1A) is an FAD-dependent amine-oxidase that demethylates mono and dimethyl histone H3 lysine 4 (H3K4Me1 and H3K4Me2). LSD1 is part of the repressor complexes involving GFI1, CoREST and HDAC1/2, that regulate active super-enhancers/enhancers (SEs/Es) and their target genes, mediating transcriptional repression and differentiation block in LSCs. GFI1 is a zinc-finger transcriptional repressor involved in AML development an

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Miles, Wayne O., Julie M. J. Lepesant, Jessie Bourdeaux, et al. "The LSD1 Family of Histone Demethylases and the Pumilio Posttranscriptional Repressor Function in a Complex Regulatory Feedback Loop." Molecular and Cellular Biology 35, no. 24 (2015): 4199–211. http://dx.doi.org/10.1128/mcb.00755-15.

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The lysine (K)-specific demethylase (LSD1) family of histone demethylases regulates chromatin structure and the transcriptional potential of genes. LSD1 is frequently deregulated in tumors, and depletion of LSD1 family members causes developmental defects. Here, we report that reductions in the expression of the Pumilio (PUM) translational repressor complex enhanced phenotypes due to dLsd1 depletion inDrosophila. We show that the PUM complex is a target of LSD1 regulation in fly and mammalian cells and that its expression is inversely correlated with LSD1 levels in human bladder carcinoma. Une

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Lin, Chiao-Yun, Chen-Bin Chang, Ren-Chin Wu, et al. "Glucose Activates Lysine-Specific Demethylase 1 through the KEAP1/p62 Pathway." Antioxidants 10, no. 12 (2021): 1898. http://dx.doi.org/10.3390/antiox10121898.

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Endometrial cancer incidence increases annually. Several risk factors, including high glucose intake, are associated with endometrial cancer. We investigated whether glucose affects lysine-specific demethylase 1 (LSD1) expression and the responsible molecular mechanisms. A high concentration of glucose stimulated p62 phosphorylation and increased LSD1 protein expression. Knockdown of p62 or treatment with mammalian target of rapamycin (mTOR), transforming growth factor-β activated kinase 1 (TAK1), casein kinase 1 (CK1), and protein kinase C (PKC) inhibitors abrogated glucose-regulated LSD1 exp

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Mosammaparast, Nima, Haeyoung Kim, Benoit Laurent, et al. "The histone demethylase LSD1/KDM1A promotes the DNA damage response." Journal of Cell Biology 203, no. 3 (2013): 457–70. http://dx.doi.org/10.1083/jcb.201302092.

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Histone demethylation is known to regulate transcription, but its role in other processes is largely unknown. We report a role for the histone demethylase LSD1/KDM1A in the DNA damage response (DDR). We show that LSD1 is recruited directly to sites of DNA damage. H3K4 dimethylation, a major substrate for LSD1, is reduced at sites of DNA damage in an LSD1-dependent manner. The E3 ubiquitin ligase RNF168 physically interacts with LSD1 and we find this interaction to be important for LSD1 recruitment to DNA damage sites. Although loss of LSD1 did not affect the initial formation of pH2A.X foci, 5

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Foster, Charles T., Oliver M. Dovey, Larissa Lezina, et al. "Lysine-Specific Demethylase 1 Regulates the Embryonic Transcriptome and CoREST Stability." Molecular and Cellular Biology 30, no. 20 (2010): 4851–63. http://dx.doi.org/10.1128/mcb.00521-10.

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ABSTRACT Lysine-specific demethylase 1 (LSD1), which demethylates mono- and dimethylated histone H3-Lys4 as part of a complex including CoREST and histone deacetylases (HDACs), is essential for embryonic development in the mouse beyond embryonic day 6.5 (e6.5). To determine the role of LSD1 during this early period of embryogenesis, we have generated loss-of-function gene trap mice and conditional knockout embryonic stem (ES) cells. Analysis of postimplantation gene trap embryos revealed that LSD1 expression, and therefore function, is restricted to the epiblast. Conditional deletion of LSD1 i

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Li, Ying, Xin Hu, River Ybarra, et al. "Serine Phosphorylation On TAL1 Regulates Its Interaction with Histone Demethylase LSD1." Blood 114, no. 22 (2009): 1460. http://dx.doi.org/10.1182/blood.v114.22.1460.1460.

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Abstract Abstract 1460 Poster Board I-483 TAL1, originally identified by virtue of its involvement in a T-cell acute lymphoblastic leukemia (T-ALL)-specific chromosomal translocation, is a member of the basic helix-loop-helix (bHLH) family of transcription factors and is required for the development of all hematopoietic cell lineages. TAL1 is a phosphorylated protein and its activities are mediated by the corepressors and coactivators that associate with TAL1. However, the functional link between phosphorylation and the recruitment of co-regulators by TAL1 is currently unknown. We undertook th

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Li, Ying, Changwang Deng, Xin Hu, Xueqi Fu, Yi Qiu, and Suming Huang. "PKA Mediated Phosphorylation of TAL1 Regulates Its Interaction with LSD1 During Hematopoiesis." Blood 116, no. 21 (2010): 2599. http://dx.doi.org/10.1182/blood.v116.21.2599.2599.

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Abstract Abstract 2599 TAL1 is a member of the basic helix-loop-helix (bHLH) family of transcription factors and is required for the development of all hematopoietic cell lineages. TAL1 is a phosphorylated protein and its activities are mediated by the corepressors and coactivators that associate with TAL1. However, the functional link between phosphorylation and the recruitment of co-regulators by TAL1 is currently unknown. We showed that TAL1 dynamically interacts with LSD1 complex containing both histone H3K4 demethylase and deacetylase activities during hematopoiesis (Proc. Natl. Acad. Sci

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Li, Mingyang, Jie Feng, Kangrong Zhao, et al. "LSD1 Demethylates and Destabilizes Autophagy Protein LC3B in Ovarian Cancer." Biomolecules 14, no. 11 (2024): 1377. http://dx.doi.org/10.3390/biom14111377.

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Autophagy is a complex cellular process that can either promote or inhibit cancer progression and development, depending on the context and molecular regulation involved. This study investigates how LSD1 regulates autophagy in ovarian cancer by interacting with the autophagy protein LC3B. Utilizing the bioinformatic analysis of TCGA, CPTAC, and GEO datasets, as well as immunohistochemistry in ovarian cancer patients, we explored the expression association between LSD1 and LC3B. Molecular mechanisms were further analyzed using Western blotting, immunoprecipitation, and GST pull-down assays. Our

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Kwok, Hui Si, Amanda Waterbury, Ceejay Lee, et al. "Differentiation of Acute Myeloid Leukemia Cells upon Pharmacological Inhibition of LSD1 Requires Its N-Terminal Intrinsically Disordered Region." Blood 142, Supplement 1 (2023): 1416. http://dx.doi.org/10.1182/blood-2023-181316.

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Lysine-specific histone demethylase 1 (LSD1/KDM1A) governs hematopoiesis by regulating hematopoietic stem cell renewal and proper differentiation. Additionally, LSD1 is required for the maintenance of acute myeloid leukemia (AML) cells and has emerged as a key therapeutic target. Prior work from our group and others have revealed that the LSD1 demethylase activity is not required for AML proliferation. Instead, the interaction between LSD1 and GFI1/GFI1B is necessary to sustain AML cell survival. Thus, beyond its canonical demethylase activity, LSD1 has nonenzymatic, transcription factor (TF)-

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Arvedson, Tara L., Lynn Tran, Sandra L. Ross, et al. "Fetal Hemoglobin Expression Is Differentially Affected by Inhibition of the Proposed Dred Complex Constituents, LSD1 and DNMT1." Blood 120, no. 21 (2012): 3263. http://dx.doi.org/10.1182/blood.v120.21.3263.3263.

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Abstract Abstract 3263 Introduction Sickle cell disease and beta thalassemia are disorders caused by mutations in adult hemoglobin (HbA) or defects in HbA expression. A potential therapeutic solution is reactivation of fetal hemoglobin (HbF) expression. Although HbF, comprising two alpha and two gamma globin chains, is the primary form of hemoglobin expressed in utero, gamma globin expression is silenced in adults. One proposed mechanism of gamma globin silencing involves binding of the direct repeat erythroid definitive (DRED) repressor complex to sequences in the gamma globin promoter. The D

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Wasson, Christopher W., Esther Perez Barreiro, Francesco Del Galdo, and Natalia A. Riobo-Del Galdo. "Lysine Demethylase 1 Has Demethylase-Dependent and Non-Canonical Functions in Myofibroblast Activation in Systemic Sclerosis." Cells 14, no. 6 (2025): 433. https://doi.org/10.3390/cells14060433.

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Systemic sclerosis (SSc) is an autoimmune disease of unknown aetiology characterised by vasculopathy with progressive fibrosis of the skin and internal organs. Tissue fibrosis is driven by activated fibroblasts (myofibroblasts) with exacerbated contractile and secretory properties. We previously reported that the long non-coding RNA HOTAIR is a key driver of SSc fibroblast activation. HOTAIR interacts with the chromatin modifiers, the polycomb repressor complex (PRC2) and coREST complex, promoting expression of pro-fibrotic genes. In this study, we show that acute activation of dermal fibrobla

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Haase, Rebecca, Andrew Groves, Hafsa Mire, Jun Qi, and Mariella Filbin. "DIPG-53. LSD1 DEGRADATION SYNERGIZES WITH HDAC INHIBITION IN PEDIATRIC H3K27M DIFFUSE MIDLINE GLIOMA." Neuro-Oncology 25, Supplement_1 (2023): i25. http://dx.doi.org/10.1093/neuonc/noad073.100.

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Abstract H3K27M-mutated diffuse midline glioma (H3K27M DMG) is an aggressive, lethal pediatric brain tumor which resists conventional cancer treatments. To identify new therapeutic targets, our lab executed a focused CRISPR negative selection screen in patient-derived H3K27M cell lines after treatment with the histone deacetylase (HDAC) inhibitor panobinostat, and discovered a strong co-dependence with the histone demethylase LSD1. We further explored the therapeutic potential of this synergistic interaction with a screen of HDAC- and LSD1- targeting drugs to identify synergistic combinations,

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Ramírez-Ramírez, Ruth, Melva Gutiérrez-Angulo, Jorge Peregrina-Sandoval, et al. "Somatic deletion of KDM1A/LSD1 gene is associated to advanced colorectal cancer stages." Journal of Clinical Pathology 73, no. 2 (2019): 107–11. http://dx.doi.org/10.1136/jclinpath-2019-206128.

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AimsKDM1A/LSD1 and ZNF217 are involved in a protein complex that participates in transcriptional regulation. ZNF217 has been analysed in numerous cancers and its amplification has been associated with advanced stages of disease; however, a similar role for KDM1A/LSD1 has not been uncovered. In this study, we estimated the number of KDM1A/LSD1 and ZNF217 gene copies in tissue samples from patients diagnosed with colorectal cancer (CRC), as well as its association with clinicopathological features in patients with CRC.MethodsParaffin-embedded tumour samples from 50 patients with CRC with a histo

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Tayari, Mina M., Tulasigeri M. Totiger, Ramin Shiekhattar, Justin Taylor, and Justin M. Watts. "The LSD1 Inhibitor Ory-1001 (ladademstat) in Combination with Menin Inhibitor SNDX-5613 (revumenib) Has Synergistic in Vitro Activity in KMT2A-Rearranged AML Models." Blood 142, Supplement 1 (2023): 5691. http://dx.doi.org/10.1182/blood-2023-190309.

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Introduction: Menin is a scaffold protein that binds to gene promoters, enhancers and transcription factors, thereby influencing transcription. Leukemias with rearrangement of KMT2A known as mixed-lineage leukemia (MLL), as well as other abnormalities such as NPM1c, respond to Menin inhibition with promising early clinical results. MLL leukemias affect children and adults and are associated with high rates of resistance to conventional chemotherapy. In addition to these alterations, other leukemia subsets with similar transcriptional dependency could be targeted through Menin inhibition. LSD1

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Subramaniam, Agatheeswaran, Kristijonas Žemaitis, Mehrnaz Safaee Talkhoncheh, et al. "Lysine-specific demethylase 1A restricts ex vivo propagation of human HSCs and is a target of UM171." Blood 136, no. 19 (2020): 2151–61. http://dx.doi.org/10.1182/blood.2020005827.

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Abstract Culture conditions in which hematopoietic stem cells (HSCs) can be expanded for clinical benefit are highly sought after. Here, we report that inhibition of the epigenetic regulator lysine-specific histone demethylase 1A (LSD1) induces a rapid expansion of human cord blood–derived CD34+ cells and promotes in vitro propagation of long-term repopulating HSCs by preventing differentiation. The phenotype and molecular characteristics of cells treated with LSD1 inhibitors were highly similar to cells treated with UM171, an agent promoting expansion of HSCs through undefined mechanisms and

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Yashar, William M., Brittany M. Smith, Jake VanCampen, et al. "Abstract 3269: Dual targeting of FLT3 and LSD1 disrupts the MYC super-enhancer complex in acute myeloid leukemia." Cancer Research 82, no. 12_Supplement (2022): 3269. http://dx.doi.org/10.1158/1538-7445.am2022-3269.

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Abstract Clinical responses to kinase inhibitor therapy in acute myeloid leukemia (AML) are limited by development of resistance. A major contributor of resistance is epigenetic adaptation to kinase inhibitor therapy. We present evidence that inhibition of the epigenetic regulator lysine-specific demethylase 1 (LSD1) augments the response to inhibitors of FMS-like tyrosine kinase 3 (FLT3) in FLT3-mutant AML. We demonstrate that combined FLT3 and LSD1 inhibition results in synergistic cell death of FLT3-mutant AML cell lines and primary patient samples. High-resolution epigenetic sequencing rev

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Lynch, James T., Gary J. Spencer, William J. Harris, et al. "Pharmacological Inhibitors of LSD1 Promote Differentiation of Myeloid Leukemia Cells through a Mechanism Independent of Histone Demethylation." Blood 124, no. 21 (2014): 267. http://dx.doi.org/10.1182/blood.v124.21.267.267.

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Abstract Lysine Specific Demethylase 1 (LSD1 or KDM1A) is one of a number of epigenetic regulators which have recently emerged as candidate therapeutic targets in acute myeloid leukaemia (AML). It is a flavin adenine dinucleotide (FAD) dependent homolog of the amine oxidase family with an ability to demethylate monomethyl or dimethyl lysine 4 (K4) of histone H3, in addition to other substrates. Pharmacological inhibitors of LSD1 such as the tranylcypromine derivatives have already commenced evaluation in early phase clinical trials. While it has been widely assumed that these compounds promote

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Gkotzamanidou, Maria, Mariateresa Fulciniti, Jesús Martín Sanchez, et al. "LSD1 Impairs the Epithelial-Mesenchymal Transition (EMT) and Osteoclastogenesis Potency in Multiple Myeloma and Synergistically Induces Cytotoxicity with HDAC Inhibitors." Blood 124, no. 21 (2014): 3410. http://dx.doi.org/10.1182/blood.v124.21.3410.3410.

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Abstract Lysine-specific demethylase 1 (LSD1) is a FAD-dependent histone demethylase, which selectively removes mono- and di-methyl groups from histone 3 lysine 4 or 9 residues (H3K4, H3K9) leading to either repression or activation of transcriptome. Previous studies have shown that lenalidomide and pomalidomide cause cell cycle arrest in Multiple Myeloma (MM) by modifying the chromatin structure of the p21WAF-1 promoter through LSD1 demethylation. LSD1 forms a co-repression complex with HDAC1 and HDAC2, mSin3a, and MMSET. However, the functional role of LSD1 in MM and its contribution in aggr

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Tang, Ming, Huangxuan Shen, Yue Jin, et al. "The Malignant Brain Tumor (MBT) Domain Protein SFMBT1 Is an Integral Histone Reader Subunit of the LSD1 Demethylase Complex for Chromatin Association and Epithelial-to-mesenchymal Transition." Journal of Biological Chemistry 288, no. 38 (2013): 27680–91. http://dx.doi.org/10.1074/jbc.m113.482349.

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Chromatin readers decipher the functional readouts of histone modifications by recruiting specific effector complexes for subsequent epigenetic reprogramming. The LSD1 (also known as KDM1A) histone demethylase complex modifies chromatin and represses transcription in part by catalyzing demethylation of dimethylated histone H3 lysine 4 (H3K4me2), a mark for active transcription. However, none of its currently known subunits recognizes methylated histones. The Snai1 family transcription factors are central drivers of epithelial-to-mesenchymal transition (EMT) by which epithelial cells acquire en

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Nicosia, Luciano, Francesca Ludovica Boffo, Elena Ceccacci, et al. "Pharmacological inhibition of LSD1 triggers myeloid differentiation by targeting GSE1 oncogenic functions in AML." Oncogene 41, no. 6 (2021): 878–94. http://dx.doi.org/10.1038/s41388-021-02123-7.

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AbstractThe histone demethylase LSD1 is over-expressed in hematological tumors and has emerged as a promising target for anticancer treatment, so that several LSD1 inhibitors are under development and testing, in preclinical and clinical settings. However, the complete understanding of their complex mechanism of action is still unreached. Here, we unraveled a novel mode of action of the LSD1 inhibitors MC2580 and DDP-38003, showing that they can induce differentiation of AML cells through the downregulation of the chromatin protein GSE1. Analysis of the phenotypic effects of GSE1 depletion in

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Yokoyama, Atsushi, Shinichiro Takezawa, Roland Schüle, Hirochika Kitagawa, and Shigeaki Kato. "Transrepressive Function of TLX Requires the Histone Demethylase LSD1." Molecular and Cellular Biology 28, no. 12 (2008): 3995–4003. http://dx.doi.org/10.1128/mcb.02030-07.

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ABSTRACT TLX is an orphan nuclear receptor (also called NR2E1) that regulates the expression of target genes by functioning as a constitutive transrepressor. The physiological significance of TLX in the cytodifferentiation of neural cells in the brain is known. However, the corepressors supporting the transrepressive function of TLX have yet to be identified. In this report, Y79 retinoblastoma cells were subjected to biochemical techniques to purify proteins that interact with TLX, and we identified LSD1 (also called KDM1), which appears to form a complex with CoREST and histone deacetylase 1.

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Gangadharan, Achintyan, Leslie Grasse, Alexsandra Espejo, et al. "EXTH-75. IN VITRO AND IN VIVO EFFICACY OF COMBINATORIAL INHIBITION OF LSD1 AND HDACS IN PATIENT DERIVED GLIOBLASTOMA STEM CELL MODELS." Neuro-Oncology 22, Supplement_2 (2020): ii103—ii104. http://dx.doi.org/10.1093/neuonc/noaa215.429.

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Abstract Inhibitors of histone deacetylases (HDACi) have been tested in glioblastoma (GBM), however, single agent clinical efficacy has not been proven, prompting study of combinatorial approaches. A rational HDACi combination strategy is with inhibition of LSD1, lysine specific demethylase 1, a histone demethylase known to exist in complex with HDAC1/2. We previously showed in vivo efficacy of combining a brain permeant LSD1 inhibitor, tranylcypromine (TCP) together with vorinostat. More selective inhibitors of LSD1 have been developed and were tested in the current study together with the HD

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Ferrarese, Roberto, Annalisa Izzo, Geoffroy Andrieux, et al. "ZBTB18 inhibits SREBP-dependent lipid synthesis by halting CTBPs and LSD1 activity in glioblastoma." Life Science Alliance 6, no. 1 (2022): e202201400. http://dx.doi.org/10.26508/lsa.202201400.

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Enhanced fatty acid synthesis is a hallmark of tumors, including glioblastoma. SREBF1/2 regulate the expression of enzymes involved in fatty acid and cholesterol synthesis. Yet, little is known about the precise mechanism regulating SREBP gene expression in glioblastoma. Here, we show that a novel interaction between the co-activator/co-repressor CTBP and the tumor suppressor ZBTB18 regulates the expression of SREBP genes. In line with our findings, metabolic assays and glucose tracing analysis confirm the reduction in several phospholipid species upon ZBTB18 expression. Our study identifies C

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Pinter, Sabine, Franziska Knodel, Michel Choudalakis, et al. "A functional LSD1 coregulator screen reveals a novel transcriptional regulatory cascade connecting R-loop homeostasis with epigenetic regulation." Nucleic Acids Research 49, no. 8 (2021): 4350–70. http://dx.doi.org/10.1093/nar/gkab180.

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Abstract The lysine specific demethylase 1 (LSD1) plays a pivotal role in cellular differentiation by regulating the expression of key developmental genes in concert with different coregulatory proteins. This process is impaired in different cancer types and incompletely understood. To comprehensively identify functional coregulators of LSD1, we established a novel tractable fluorescent reporter system to monitor LSD1 activity in living cells. Combining this reporter system with a state-of-the-art multiplexed RNAi screen, we identify the DEAD-box helicase 19A (DDX19A) as a novel coregulator an

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Chau, Charles M., Zhong Deng, Hyojueng Kang, and Paul M. Lieberman. "Cell Cycle Association of the Retinoblastoma Protein Rb and the Histone Demethylase LSD1 with the Epstein-Barr Virus Latency Promoter Cp." Journal of Virology 82, no. 7 (2008): 3428–37. http://dx.doi.org/10.1128/jvi.01412-07.

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ABSTRACT The Epstein-Barr virus C promoter (Cp) regulates the major multicistronic transcript encoding the EBNA-LP, 1, 2, and 3 genes required for B-cell proliferation during latency. The growth-transforming potential of these viral genes suggests that they must be tightly regulated with the host cell cycle and differentiation process. To better understand Cp regulation, we used DNA affinity purification to identify cellular and viral proteins that bind to Cp in latently infected cells. Several previously unknown factors were identified, including the cell cycle regulatory proteins E2F1 and Rb

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S, Dhanalakshmi, Sridharan Rajagopal, Naveen Sadhu, et al. "Novel Dual Inhibitor of LSD1-HDAC6/8 for Treatment of Cancer." Blood 136, Supplement 1 (2020): 29. http://dx.doi.org/10.1182/blood-2020-142685.

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Introduction: Lysine specific demethylase 1 (LSD1) and histone deacetylases (HDACs) are known to modulate the expression of several disease specific genes as part of repressor complexes, including CoREST. In addition, they also have complex mutually exclusive roles in cancer cells. Accordingly, several studies have shown that combined inhibition of these proteins to have a profound effect in inhibiting tumor growth. In this regard, although class I HDAC inhibition has been well studied, dose limiting toxicities associated with these inhibitors is still a challenge in the clinic, it has been hy

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Nguyen, Minh N., Hirokazu Taniguchi, Andrew Chow, Yingqian A. Zhan, Triparna Sen, and Charles M. Rudin. "Abstract 1370: Targeting LSD1 rescues MHC-I antigen presentation in small cell lung cancer." Cancer Research 82, no. 12_Supplement (2022): 1370. http://dx.doi.org/10.1158/1538-7445.am2022-1370.

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Abstract Purpose: Small cell lung cancer (SCLC) is a highly aggressive cancer with early primary resistance and modest clinical benefit to immune checkpoint blockade (ICB). Mutation or transcriptional repression of the major histocompatibility complex class I (MHC-I) is a key mechanism driving resistance to T cell-based therapies. Lysine Demethylase 1 (LSD1) regulates gene expression through modulating mono- and di- methylated lysine 4 and 9 of histone H3. LSD1 is a therapeutic target of interests in SCLC due to its oncogenic requirement for tumor growth, and there has been growing evidence po

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Groves, Andrew, Rebecca Poetschke, Hafsa Mire, et al. "DIPG-26. Targeted Protein Degradation of LSD1 synergizes with HDAC inhibitors in Diffuse Intrinsic Pontine Glioma." Neuro-Oncology 24, Supplement_1 (2022): i24. http://dx.doi.org/10.1093/neuonc/noac079.083.

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Abstract Diffuse intrinsic pontine glioma (DIPG) remains one of the most lethal brain tumors in all of childhood with no effective treatments besides radiation, which only extends survival a few months. Against this backdrop, our lab recently executed a focused CRISPR negative selection screen in DIPG cell lines after treatment with the histone deacetylase (HDAC) inhibitor panobinostat and discovered a strong co-dependence with the histone demethylase LSD1. To further explore the therapeutic potential of this synergistic interaction, we tested a drug library of HDAC- and LSD1- targeting drugs

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Ladaika, Christopher A., Ahmed H. Ghobashi, William C. Boulton, and Heather M. O'Hagan. "Abstract 1690: LSD1 and CoREST2 demethylate STAT3 to promote enteroendocrine cell differentiation in mucinous colorectal cancer." Cancer Research 84, no. 6_Supplement (2024): 1690. http://dx.doi.org/10.1158/1538-7445.am2024-1690.

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Abstract Across different cancer types, tumor heterogeneity has been shown to drive tumor progression, metastasis, and therapeutic resistance. Adenocarcinoma to neuroendocrine lineage transition is an emergent mechanism of targeted therapy resistance in several cancer types, including lung and prostate cancer. Therefore, understanding the dynamics and mechanisms driving neuroendocrine cell fates in cancer is critical. Mucinous colorectal cancer accounts for upwards of 20% of colorectal cancer cases and is characterized by tumors with mucous accounting for at least 50% of the tumor volume. The

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Johnston, Gretchen, Haley E. Ramsey, Kristy Stengel, et al. "Nascent Transcript and Single Cell Rnaseq Analysis Defines the Mechanism of Action of the LSD1 Inhibitor INCB059872 in Myeloid Leukemia." Blood 134, Supplement_1 (2019): 2509. http://dx.doi.org/10.1182/blood-2019-130458.

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Drugs targeting chromatin-modifying enzymes have entered clinical trials for myeloid malignancies, including INCB059872, a selective irreversible inhibitor of Lysine-Specific Demethylase 1 (LSD1). LSD1 is a component of the CoREST complex, in which it associates with histone deacetylases 1 and 2, the transcriptional co-repressor, mSin3A or mSin3B, and the REST corepressor (RCOR1), so a role in gene expression was expected. While initial studies of LSD1 inhibitors have suggested these compounds may be used to induce differentiation of acute myeloid leukemia, the mechanisms underlying this effec

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Lone, Mehraju Din, Mohd Sayeed, Alaa Habieb, Praveen Kumar, and Michael E. Engel. "Abstract 5630: Targeting the LSD1/ADNP axis as an effective pro-differentiating strategy against acute myeloid leukemia AML." Cancer Research 84, no. 6_Supplement (2024): 5630. http://dx.doi.org/10.1158/1538-7445.am2024-5630.

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Abstract Acute Myeloid Leukemia (AML) represents a diverse category of blood cancers marked by the clonal proliferation of atypical myeloid precursor cells within the bone marrow. Lysine Specific Demethylase 1 (LSD1), an epigenetic regulator, exhibits elevated expression in AML. Consequently, inhibiting LSD1 has emerged as a promising therapeutic approach for addressing blood and bone marrow cancers. While initial emphasis centered on LSD1's enzymatic inhibition, compelling evidence highlights its pivotal role as a scaffolding protein, orchestrating transcriptional and chromatin remodeling com

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35

Barnes, Claire E., David M. English, Megan Broderick, Mark O. Collins, and Shaun M. Cowley. "Proximity-dependent biotin identification (BioID) reveals a dynamic LSD1–CoREST interactome during embryonic stem cell differentiation." Molecular Omics 18, no. 1 (2022): 31–44. http://dx.doi.org/10.1039/d1mo00236h.

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36

Barnes, Claire E., David M. English, Megan Broderick, Mark O. Collins, and Shaun M. Cowley. "Proximity-dependent biotin identification (BioID) reveals a dynamic LSD1–CoREST interactome during embryonic stem cell differentiation." Molecular Omics 18, no. 1 (2022): 31–44. http://dx.doi.org/10.1039/d1mo00236h.

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37

Yu, Lei, Yu Wang, Richard King, et al. "The LSD1 Inhibitor RN1 Rescues Congenital Dyserythropoietic Anemia Type II." Blood 144, Supplement 1 (2024): 938. https://doi.org/10.1182/blood-2024-201649.

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Congenital dyserythropoietic anemia type II (CDAII) is an autosomal recessive disease resulting from loss-of-function mutations in SEC23B, which encodes a component of coat complex protein II (COPII) vesicles. Mammals express two paralogous genes for SEC23, SEC23A and SEC23B, which encode proteins with ~85% amino acid sequence identity. We have previously shown that the SEC23 paralogs have identical interactomes and that SEC23A overlaps in function with SEC23B. Since the SEC23B/SEC23A expression ratio is disproportionately high in human erythroid cells, we reasoned that the endogenous SEC23A e

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Jin, Yue, Yidi Guo, Dongxue Liang, Yue Li, Zhe Li, and Xin Hu. "LSD1 Plays an Important Role in GATA Switch during Erythroid Differentiation." Blood 122, no. 21 (2013): 4846. http://dx.doi.org/10.1182/blood.v122.21.4846.4846.

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Abstract GATA factors play important role in hematopoiesis. In particular, GATA2 is critical for maintenance of hematopoietic stem and progenitor cells (HS/PCs) and GATA1 is required for erythropoiesis. GATA1 and GATA2 are expressed in reciprocal patterns during erythroid differentiation. It was shown that GATA1 occupied the -2.8Kb regulatory element and mediated repression of the GATA2 promoter in terminally differentiating erythroid cells. However, the detailed molecular mechanisms that control the enhancer/promoter activities of the GATA2 gene remain to be elucidated. In this report, we fou

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39

Pezone, Antonio, Maria Letizia Taddei, Alfonso Tramontano та ін. "Targeted DNA oxidation by LSD1–SMAD2/3 primes TGF-β1/ EMT genes for activation or repression". Nucleic Acids Research 48, № 16 (2020): 8943–58. http://dx.doi.org/10.1093/nar/gkaa599.

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Abstract The epithelial-to-mesenchymal transition (EMT) is a complex transcriptional program induced by transforming growth factor β1 (TGF-β1). Histone lysine-specific demethylase 1 (LSD1) has been recognized as a key mediator of EMT in cancer cells, but the precise mechanism that underlies the activation and repression of EMT genes still remains elusive. Here, we characterized the early events induced by TGF-β1 during EMT initiation and establishment. TGF-β1 triggered, 30–90 min post-treatment, a nuclear oxidative wave throughout the genome, documented by confocal microscopy and mass spectrom

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Fiskus, Warren, Sunil Sharma, Sunil Abhyankar, Joseph McGuirk, David J. Bearss, and Kapil Bhalla. "Pre-Clinical Efficacy of Combined Therapy with LSD1 Antagonist SP-2509 and Pan-Histone Deacetylase Inhibitor Against AML Blast Progenitor Cells." Blood 120, no. 21 (2012): 868. http://dx.doi.org/10.1182/blood.v120.21.868.868.

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Abstract Abstract 868 LSD1 (KDM1A) is an FAD-dependent histone demethylase, with homology to amine oxidases. LSD1 demethylates di- and mono-methylated lysine (K) 4 on histone H3, reducing the permissive H3K4Me3 chromatin mark for gene expression. LSD1 forms a complex with the histone deacetylases (HDAC) 1 and 2 and with the co-repressor CoREST, which stimulates the activity of LSD1 toward nucleosomes. While high LSD1 expression may be an effector of blocked differentiation and confers poor prognosis in AML, LSD1 inhibition induces the expression of myeloid–differentiation associated genes and

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Fiskus, Warren, Sunil Sharma, Rekha Rao, et al. "Combined Targeting of Chromatin Modifying Enzymes LSD1, EZH2 and Histone Deacetylases (HDACs) Has Superior Efficacy Against Human Mantle Cell Lymphoma Cells." Blood 118, no. 21 (2011): 2429. http://dx.doi.org/10.1182/blood.v118.21.2429.2429.

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Abstract Abstract 2429 PRC (polycomb repressive complex) 2 contains three core protein components, i.e., EZH2, SUZ12 and EED, of which EZH2 has the SET domain with its intrinsic histone methyltransferase activity that mediates the trimethylation (Me3) of lysine (K) 27 on histone (H) 3-a repressive chromatin mark for gene expression. We have previously reported that treatment with the S-adenosylhomocysteine hydrolase and EZH2 inhibitor, DZNep as well as treatment with the pan-histone deacetylase inhibitor panobinostat (PS, Novartis Pharma) deplete PRC2 complex proteins. LSD1 (KDM1A) is a demeth

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Kerenyi, Marc A., Jessica Hsu, Zhen Shao, and Stuart H. Orkin. "Histone Demethylase LSD1 Is Required to Repress Hematopoietic Stem Cell Signatures in Mature Blood Cells to Permit Terminal Differentiation." Blood 118, no. 21 (2011): 550. http://dx.doi.org/10.1182/blood.v118.21.550.550.

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Abstract Abstract 550 Lysine specific demethylase 1 (LSD1) is a demethylase that acts on mono- and dimethylated H3K4 (H3K4me1/2). Consistent with H3K4me2 (an active marker of transcription) as a substrate, LSD1 is part of a core complex with the co-repressor, CoREST and HDAC1/2. Previously our lab demonstrated that regulation of hematopoietic differentiation depends in part on the interaction of the growth factor independent transcription factors (= Gfi1 and Gfi1b) with the LSD1/CoREST/HDAC complex. We generated a conditional knock out mouse for LSD1 (LSD1fl/fl) to study its roles in hematopoi

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Dohrmann, Paul R., Guy Oshiro, Marianne Tecklenburg, and Robert A. Sclafani. "RAD53 Regulates DBF4 Independently of Checkpoint Function in Saccharomyces cerevisiae." Genetics 151, no. 3 (1999): 965–77. http://dx.doi.org/10.1093/genetics/151.3.965.

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Abstract The Cdc7p and Dbf4p proteins form an active kinase complex in Saccharomyces cerevisiae that is essential for the initiation of DNA replication. A genetic screen for mutations that are lethal in combination with cdc7-1 led to the isolation of seven lsd (lethal with seven defect) complementation groups. The lsd7 complementation group contained two temperature-sensitive dbf4 alleles. The lsd1 complementation group contained a new allele of RAD53, which was designated rad53-31. RAD53 encodes an essential protein kinase that is required for the activation of DNA damage and DNA replication

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44

Goossens, Steven, Sofie Peirs, Geert Berx, Pieter Van Vlierberghe, and Jody J. Haigh. "Oncogenic ZEB2 Activation Drives Sensitivity Towards LSD1 Inhibition in T-Cell Acute Lymphoblastic Leukemia." Blood 128, no. 22 (2016): 4027. http://dx.doi.org/10.1182/blood.v128.22.4027.4027.

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Abstract T-cell acute lymphoblastic leukemias (T-ALLs) are rare aggressive hematologic tumors resulting from the malignant transformation of T-cell progenitors. The prognosis of T-ALL has gradually improved with the introduction of intensified chemotherapy. However, the outcome of T-ALL patients with primary resistant or relapsed leukemia remains extremely poor. Therefore, current research efforts are focused on the development of more effective and less toxic anti-leukemic drugs, which will likely require an improved understanding of the molecular biology of chemotherapy resistant residual tu

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45

Deb, Gauri, Bettina Wingelhofer, Emma Williams, Hui-Sun Leong, and Tim CP Somervaille. "Genome-Wide CRISPR-Cas9 Screen Identifies Sensitizers to LSD1 Inhibition in MLL-Translocated Human AML Cells." Blood 132, Supplement 1 (2018): 178. http://dx.doi.org/10.1182/blood-2018-178.

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Abstract Lysine-specific demethylase (LSD1, also known as KDM1A) is an epigenetic regulator that has recently emerged as a potential therapeutic target in acute myeloid leukemia (AML). It is a flavin dependent monoamine oxidase which can demethylate monomethyl or dimethyl lysine 4 of histone H3. Pharmacological inhibition of LSD1 induces differentiation of blast cells in MLL-translocated AML and has shown significant promise in pre-clinical studies. With LSD1 inhibitors advancing through early-phase clinical trials, there is a strong pre-clinical rationale for the identification of genes whose

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46

Getman, Michael, Samantha J. England, James Palis, and Laurie A. Steiner. "Inhibition of LSD1 Influences Multiple Mechanisms of Epigenetic Gene Regulation During Terminal Erythroid Maturation." Blood 120, no. 21 (2012): 3442. http://dx.doi.org/10.1182/blood.v120.21.3442.3442.

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Abstract Abstract 3442 The maturation of a committed erythroid progenitor to a functional red blood cell is a complex process involving significant changes in gene expression during a time of rapid cell division and nuclear condensation. LSD1 (Lysine-Specific Histone Demethylase 1) is a histone H3 lysine 4 (H3K4) and lysine 9 (H3K9) demethylase that plays pivotal role in this process. LSD1 participates in both enhancer and repressor complexes, and facilitates repression of γ-globin by participating in the Direct Repeat Erythroid Complex (Cui, MCB, 2011). LSD1 inhibitors Tranylcypromine (TCP) a

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Maiques-Diaz, Alba, James T. Lynch, Gary J. Spencer, and Tim C. P. Somervaille. "LSD1 inhibitors disrupt the GFI1 transcription repressor complex." Molecular & Cellular Oncology 5, no. 4 (2018): e1481813. http://dx.doi.org/10.1080/23723556.2018.1481813.

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48

Kim, Kyounghyun, and Ponmari Guruvaiya. "Abstract 440: Dual epigenetic targeting of hepatocellular carcinoma." Cancer Research 85, no. 8_Supplement_1 (2025): 440. https://doi.org/10.1158/1538-7445.am2025-440.

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Abstract Despite advancements in medical treatment, hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality globally. Combination therapies involving multiple targeted agents are increasingly recognized as effective strategies to improve treatment outcomes and overcome the limitations of single-agent therapies. While single-target approaches have shown specificity and potency, they face challenges such as drug resistance, limited pharmacokinetics, and patient adherence. Given the complex nature of HCC, targeting multiple molecular pathways through combination strateg

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Olsson, H. Andre, Andrew Plassard, Phillip Dexheimer, et al. "Next Gen Dissection of Gfi1 Dependent Transcriptome in Myeloid Progenitors Reveals Global Control of Multiple Transcriptional Programs Including Coding and Non Coding RNAs." Blood 120, no. 21 (2012): 111. http://dx.doi.org/10.1182/blood.v120.21.111.111.

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Abstract Abstract 111 Growth Factor Independence 1 (Gfi1) is a regulator of HSC maintenance, and lack of Gfi1 leads to myeloid progenitor accumulation and neutropenia. The Gfi1 transcription factor contains both a SNAG repressor domain, and a zinc-finger DNA-binding domain. A proline to alanine substitution at position 2 in the SNAG domain (P2A) blocks RCoR/Lysine Specific Demethylase 1 (LSD1) interaction and abrogates Gfi1-mediated repression. Mouse models have been developed which either delete Gfi1 exons 2–3 (Gfi1Δex2-3) or knock in the P2A mutation (GfiP2A). Both models are neutropenic, an

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Fiskus, Warren, Sunil Sharma, Rekha Rao, et al. "Combined targeting of LSD1 (KDM1A) and histone deacetylases exerts superior efficacy against human AML." Journal of Clinical Oncology 30, no. 15_suppl (2012): 10549. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.10549.

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10549 Background: LSD1 (KDM1A) is FAD-dependent histone H3K4Me2 demethylase. Inhibition of LSD1 increases H3K4Me3-a permissive mark for gene expression, and inhibits growth of pluripotent cancer cells. We have previously noted that treatment with the histone deacetylase (HDAC) inhibitor panobinostat (PS) depletes EZH2 (the catalytic subunit of the polycomb repressive complex 2, PRC2) and disrupts its interaction with the other PRC2 proteins, attenuates LSD1, and de-represses growth inhibitory and pro-apoptosis genes. Methods: In the present studies, we determined the chromatin effects and the

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