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Journal articles on the topic 'Complexo LSD1/CoREST'

Author: Grafiati

Published: 4 September 2021

Last updated: 29 July 2025

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

Gu, Haidong, and Bernard Roizman. "Engagement of the Lysine-Specific Demethylase/HDAC1/CoREST/REST Complex by Herpes Simplex Virus 1." Journal of Virology 83, no. 9 (2009): 4376–85. http://dx.doi.org/10.1128/jvi.02515-08.

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ABSTRACT Among the early events in herpes simplex virus 1 replication are localization of ICP0 in ND10 bodies and accumulation of viral DNA-protein complexes in structures abutting ND10. ICP0 degrades components of ND10 and blocks silencing of viral DNA, achieving the latter by dislodging HDAC1 or -2 from the lysine-specific demethylase 1 (LSD1)/CoREST/REST repressor complex. The role of this process is apparent from the observation that a dominant-negative CoREST protein compensates for the absence of ICP0 in a cell-dependent fashion. HDAC1 or -2 and the CoREST/REST complex are independently

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10

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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11

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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12

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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13

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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14

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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15

Geethadevi, Anupa, Marianne Collard, Nikhil Vaidya, et al. "ATRT-04. TARGETING THE COREST COMPLEX HELPS REPROGRAM AT/RT’S ABNORMAL EPIGENETIC LANDSCAPE TOWARD A DIFFERENTIATION PHENOTYPE." Neuro-Oncology 25, Supplement_1 (2023): i1—i2. http://dx.doi.org/10.1093/neuonc/noad073.004.

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Abstract Atypical teratoid/rhabdoid tumors (AT/RT) are deadly infantile brain tumors. Their aggressive phenotype results from a single recurring biallelic loss-of-function mutation in genes encoding components of the SWI/SNF chromatin-remodeling complex - mainly SMARCB1 and SMARCA4 in remaining tumors. Residual SWI/SNF activity continues to inhibit EZH2 methyltransferase except at promoter regions colocalized to REST, which associates with neuronal differentiation and tumor suppressor genes. At these sites, EZH2 increases repressive H3K27me3 marks, helping maintain AT/RT in a stem cell-like st

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16

Chen, Kai, Yuanxia Cai, Cheng Cheng, et al. "MYT1 attenuates neuroblastoma cell differentiation by interacting with the LSD1/CoREST complex." Oncogene 39, no. 21 (2020): 4212–26. http://dx.doi.org/10.1038/s41388-020-1268-6.

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17

Kim, Sang-Ah, Nilanjana Chatterjee, Matthew J. Jennings, Blaine Bartholomew, and Song Tan. "Extranucleosomal DNA enhances the activity of the LSD1/CoREST histone demethylase complex." Nucleic Acids Research 43, no. 10 (2015): 4868–80. http://dx.doi.org/10.1093/nar/gkv388.

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18

Dhall, Abhinav, Caroline E. Weller, Aurea Chu, Patrick M. M. Shelton, and Champak Chatterjee. "Chemically Sumoylated Histone H4 Stimulates Intranucleosomal Demethylation by the LSD1–CoREST Complex." ACS Chemical Biology 12, no. 9 (2017): 2275–80. http://dx.doi.org/10.1021/acschembio.7b00716.

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19

Curtis, Brenda J., Claudia B. Zraly та Andrew K. Dingwall. "Drosophila LSD1-CoREST demethylase complex regulates DPP/TGFβ signaling during wing development". genesis 51, № 1 (2012): 16–31. http://dx.doi.org/10.1002/dvg.22346.

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20

Geethadevi, Anupa, Marianne Collard, Tyler Findlay, et al. "Abstract 7555: Selective inhibition of the CoREST complex as a novel therapeutic target of atypical teratoid rhabdoid tumors." Cancer Research 84, no. 6_Supplement (2024): 7555. http://dx.doi.org/10.1158/1538-7445.am2024-7555.

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Abstract Atypical teratoid/rhabdoid tumors (AT/RT) are deadly infantile brain tumors, primarily arising from a single recurring biallelic loss-of-function mutation in SMARCB1 which is a member of the SWI-SNF chromatin remodeling complex. The partially functional SWI-SNF complex (without SMARCB1) is able to inhibit EZH2 at most locations of the genome except at gene promoter regions where EZH2 co-localizes with the REST complex. This results in hypermethylation and subsequent repression of genes coding for neuronal differentiation and tumor suppressors. CoREST is an important transcriptional re

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21

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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22

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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23

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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Geethadevi, Anupa, Marianne Collard, Nikhil Vaidya, et al. "Abstract 1141: The CoREST complex as a novel target to disrupt AT/RT’s abnormal epigenetic landscape." Cancer Research 83, no. 7_Supplement (2023): 1141. http://dx.doi.org/10.1158/1538-7445.am2023-1141.

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Abstract Atypical teratoid/rhabdoid tumors (AT/RT) are deadly infantile brain tumors. Their aggressive phenotype results from a single recurring biallelic loss-of-function mutation in genes encoding components of the SWI/SNF chromatin-remodeling complex - SMARCB1 in the majority of tumors and SMARCA4 in remaining tumors. Residual SWI/SNF activity continues to inhibit EZH2 methyltransferase except at gene promoter regions where EZH2 co-localizes with the REST complex. At these sites, EZH2 increases repressive H3K27me3 marks. EZH2 co-localizes with REST on neuronal differentiation and tumor supp

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25

Song, Yun, Lisbeth Dagil, Louise Fairall, et al. "Mechanism of Crosstalk between the LSD1 Demethylase and HDAC1 Deacetylase in the CoREST Complex." Cell Reports 30, no. 8 (2020): 2699–711. http://dx.doi.org/10.1016/j.celrep.2020.01.091.

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26

Lopez, Cecilia I., Katherine E. Saud, Rodrigo Aguilar, et al. "The chromatin modifying complex CoREST/LSD1 negatively regulates notch pathway during cerebral cortex development." Developmental Neurobiology 76, no. 12 (2016): 1360–73. http://dx.doi.org/10.1002/dneu.22397.

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27

Sobczak, Maciej, Magdalena Strachowska, Karolina Gronkowska, and Agnieszka Robaszkiewicz. "Activation of ABCC Genes by Cisplatin Depends on the CoREST Occurrence at Their Promoters in A549 and MDA-MB-231 Cell Lines." Cancers 14, no. 4 (2022): 894. http://dx.doi.org/10.3390/cancers14040894.

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Although cisplatin-based therapies are common among anticancer approaches, they are often associated with the development of cancer drug resistance. This phenomenon is, among others, caused by the overexpression of ATP-binding cassette, membrane-anchored transporters (ABC proteins), which utilize ATP to remove, e.g., chemotherapeutics from intracellular compartments. To test the possible molecular basis of increased expression of ABCC subfamily members in a cisplatin therapy mimicking model, we generated two cisplatin-resistant cell lines derived from non-small cell lung cancer cells (A549) an

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28

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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29

Gocke, Christian B., and Hongtao Yu. "ZNF198 Stabilizes the LSD1–CoREST–HDAC1 Complex on Chromatin through Its MYM-Type Zinc Fingers." PLoS ONE 3, no. 9 (2008): e3255. http://dx.doi.org/10.1371/journal.pone.0003255.

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30

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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31

Baron, Riccardo, Claudia Binda, Marcello Tortorici, J. Andrew McCammon, and Andrea Mattevi. "Molecular Mimicry and Ligand Recognition in Binding and Catalysis by the Histone Demethylase LSD1-CoREST Complex." Structure 19, no. 2 (2011): 212–20. http://dx.doi.org/10.1016/j.str.2011.01.001.

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32

Ouyang, Jian, Yujiang Shi, Alvaro Valin, Yan Xuan, and Grace Gill. "Direct Binding of CoREST1 to SUMO-2/3 Contributes to Gene-Specific Repression by the LSD1/CoREST1/HDAC Complex." Molecular Cell 34, no. 2 (2009): 145–54. http://dx.doi.org/10.1016/j.molcel.2009.03.013.

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Ceballos-Chavez, M., S. Rivero, P. Garcia-Gutierrez, et al. "Control of neuronal differentiation by sumoylation of BRAF35, a subunit of the LSD1-CoREST histone demethylase complex." Proceedings of the National Academy of Sciences 109, no. 21 (2012): 8085–90. http://dx.doi.org/10.1073/pnas.1121522109.

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Kuppuswamy, M., S. Vijayalingam, Ling-Jun Zhao, et al. "Role of the PLDLS-Binding Cleft Region of CtBP1 in Recruitment of Core and Auxiliary Components of the Corepressor Complex." Molecular and Cellular Biology 28, no. 1 (2007): 269–81. http://dx.doi.org/10.1128/mcb.01077-07.

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ABSTRACT C-terminal binding protein (CtBP) family proteins CtBP1 and CtBP2 are highly homologous transcriptional corepressors and are recruited by a large number of transcription factors to mediate sequence-specific transcriptional repression. In addition to DNA-binding repressors, the nuclear protein complex of CtBP1 consists of enzymatic constituents such as histone deacetylases (HDAC1/2), histone methyl transferases (HMTases; G9a and GLP), and the lysine-specific demethylase (LSD1). Additionally, CtBPs also recruit the components of the sumoylation machinery. The CtBPs contain two different

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35

Noches, Verónica, Carlos Rivera, Marcela P. González, Gianluca Merello, Montserrat Olivares-Costa, and María Estela Andrés. "Pilocarpine-induced seizures associate with modifications of LSD1/CoREST/HDAC1/2 epigenetic complex and repressive chromatin in mice hippocampus." Biochemistry and Biophysics Reports 25 (March 2021): 100889. http://dx.doi.org/10.1016/j.bbrep.2020.100889.

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36

Geethadevi, Anupa, Marianne Collard, Tyler Findlay, et al. "ATRT-14. TARGETING ATYPICAL TERATOID RHABDOID TUMORS USING A NOVEL BI-FUNCTIONAL COREST INHIBITOR." Neuro-Oncology 26, Supplement_4 (2024): 0. http://dx.doi.org/10.1093/neuonc/noae064.014.

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Abstract BACKGROUND Atypical teratoid/rhabdoid tumors (ATRT) are deadly infantile brain tumors driven by a loss-of-function mutation of SMARCB1, a critical component of the SWI-SNF chromatin remodeling complex. However, residual SWI-SNF activity inhibits EZH2 at all loci except where CoREST colocalizes with these complexes, specifically contributing to ATRT pathogenesis. This results in hypermethylation and subsequent repression of genes coding for neuronal differentiation and tumor suppressors, accounting for ATRTs’ stem-like state, aggressive growth, and therapy resistance. We functionally i

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Dutta, Sayanika, Girijesh Kumar Patel, Hamed Khedmatgozar, et al. "Abstract 6603: A TBX2-driven signaling switch from androgen receptor to glucocorticoid receptor confers enzalutamide resistance in prostate cancer." Cancer Research 84, no. 6_Supplement (2024): 6603. http://dx.doi.org/10.1158/1538-7445.am2024-6603.

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Abstract Background: Recent studies suggest that glucocorticoid receptor (GR) activation can cause enzalutamide resistance in advanced prostate cancer (PCa) via functional bypass of androgen receptor (AR) signaling. However, the specific molecular mechanism(s) driving this process remain unknown. In an effort to identify drivers of prostate cancer progression, in a previous study, we determined that TBX2, a developmental T-box transcription factor (TF) master regulator, is over-expressed in CRPC and drives bone metastatic progression. A recent report confirmed that TBX2 and GR are two of the f

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Roizman, B. "The Checkpoints of Viral Gene Expression in Productive and Latent Infection: the Role of the HDAC/CoREST/LSD1/REST Repressor Complex." Journal of Virology 85, no. 15 (2011): 7474–82. http://dx.doi.org/10.1128/jvi.00180-11.

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39

Laurent, Benoît, Voahangy Randrianarison-Huetz, Emilie Frisan, et al. "A short Gfi-1B isoform controls erythroid differentiation by recruiting the LSD1–CoREST complex through the dimethylation of its SNAG domain." Journal of Cell Science 125, no. 4 (2012): 993–1002. http://dx.doi.org/10.1242/jcs.095877.

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Zalloum, Waleed A., and Hiba M. Zalloum. "Exploring the Active Center of the LSD1/CoREST Complex by Molecular Dynamics Simulation Utilizing Its Co-crystallized Co-factor Tetrahydrofolate as a Probe." Journal of Chemical Information and Modeling 57, no. 12 (2017): 3022–31. http://dx.doi.org/10.1021/acs.jcim.7b00256.

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Muench, David E., Chinavenmeni S. Velu, Andre Olsson, Sara E. Meyer, and H. Leighton Grimes. "Transcriptional Control of HSC Fitness." Blood 126, no. 23 (2015): 1161. http://dx.doi.org/10.1182/blood.v126.23.1161.1161.

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Abstract To sustain lifetime hematopoiesis, adult hematopoietic stem cells (HSCs) are required to remain quiescent. Proper control over cell cycle status underlies HSC fitness. Although the identity of cell cycle mediators which control HSC cycling are basically understood, the gene regulatory networks controlling them are largely unknown. Gfi1 encodes a transcriptional repressor protein that is required to maintain HSC quiescence. Over-cycling of stem-progenitors causes Gfi1-/- HSC exhaustion and prevents long-term engraftment in lethally-ablated recipients. Gfi1 controls myeloid progenitor m

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Butera, Ambra, Antonio Gennaro Nicotera, Gabriella Di Rosa, et al. "PHF21A Related Disorder: Description of a New Case." International Journal of Molecular Sciences 23, no. 24 (2022): 16130. http://dx.doi.org/10.3390/ijms232416130.

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PHF21A (PHD finger protein 21A) gene, located in the short arm of chromosome 11, encodes for BHC80, a component of the Lysine Specific Demethylase 1, Corepressor of REST (LSD1-CoREST) complex. BHC80 is mainly expressed in the human fetal brain and skeletal muscle and acts as a modulator of several neuronal genes during embryogenesis. Data from literature relates PHF21A variants with Potocki–Shaffer Syndrome (PSS), a contiguous gene deletion disorder caused by the haploinsufficiency of PHF21A, ALX4, and EXT2 genes. Clinical cardinal features of PSS syndrome are multiple exostoses (due to the EX

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Tellechea, Maria Florencia Florencia, Jalila Chagraoui, Nadine Mayotte, and Guy Sauvageau. "Deciphering the Boundaries of KBTBD4-CoREST1 Axis Modulation to Maximally Expand Human HSCs." Blood 142, Supplement 1 (2023): 2681. http://dx.doi.org/10.1182/blood-2023-189646.

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Background: The UM171 technology has led to major progress in the expansion of cord blood units (CBUs) with low cellularity (Fares et al., Science 2014). This breakthrough has notably increased availability of better HLA-matched CBUs and improvements in clinical outcome (Cohen et al., Lancet Hematol 2020 and Blood Advances 2023, PMID: 37467030; see also Cohen et al. and Milano et al., this meeting). Enhanced HLA matching is a direct consequence of the selection of CBUs which are otherwise too small without expansion. Indeed, with this technology, approximately 50% of units in CB banks are elig

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Shooshtarizadeh, Peiman, Ryan Chen, and Tarik Moroy. "The Zinc Finger Transcription Factor Growth Factor Independence 1b (Gfi1b) Regulates The Wnt/Beta-Catenin Signaling Pathway In Hematopoietic Stem Cells Through Interaction With Inhibitory Proteins." Blood 122, no. 21 (2013): 2417. http://dx.doi.org/10.1182/blood.v122.21.2417.2417.

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Abstract Hematopoietic stem cells (HSCs) reside in the bone marrow in specific niches at the border between bone cells and the bone marrow (endosteal niche) or around blood vessels (perivascular niche). In the endosteal niche, HSCs are maintained at low oxygen levels in a quiescent (dormant) state by adhesion to niche cells. We have previously shown that Gfi1b restricts the expansion and proliferation of HSCs as well as their mobilization or re-localization into peripheral blood. We have proposed that Gfi1b exerts this function by regulating the expression of surface molecules such as integrin

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Balaji, Swapnaa, Rabin Neupane, Chandrabose Karthikeyan, Jayachandra Babu Ramapuram, and Amit K. Tiwari. "Abstract 4974: Development of novel pyrimido-pyrazolo-quinolone derivative, IND-2 as multi-targeted inhibitor for the treatment of prostate cancer." Cancer Research 83, no. 7_Supplement (2023): 4974. http://dx.doi.org/10.1158/1538-7445.am2023-4974.

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Abstract Prostate cancer (PC) is the most commonly diagnosed cancer in men. In PC, multiple molecular signaling networks are perturbed, so monotherapies are less effective, creating an urgent need to discover chemotherapeutic agents that target multiple tumor-promoting proteins simultaneously. Drug discovery research is increasingly embracing poly-pharmacology, in which one drug targets multiple oncogenic targets concurrently. We have identified a novel quinoline derivative, IND-2 (4-chloro-2-methylpyrimido[1″,2″:1,5]pyrazolo[3,4-b]quinolone), that has been shown to significantly inhibit the e

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Zhou, Guoying, Du Te, and Bernard Roizman. "The CoREST/REST Repressor Is both Necessary and Inimical for Expression of Herpes Simplex Virus Genes." mBio 2, no. 1 (2010). http://dx.doi.org/10.1128/mbio.00313-10.

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ABSTRACTHerpes simplex virus type 1 encodes three sets of genes, α, β, and γ, whose expression is sequentially ordered in a cascade fashion. The transactivators of α genes comprise virion protein 16 (VP16) and the cellular proteins octamer binding protein 1 (Oct1) and host factor 1 (HCF1). Efficient transition from α to β gene expression requires the α protein ICP0 (infected cell protein 0). Earlier studies have shown that this protein binds to CoREST and displaces HDAC1 from the CoREST/REST/lysine-specific demethylase 1 (LSD1) repressor complex. Ultimately, the components of the repressor com

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Gahan, James M., Lucas Leclère, Maria Hernandez-Valladares, and Fabian Rentzsch. "A developmental role for the chromatin-regulating CoREST complex in the cnidarian Nematostella vectensis." BMC Biology 20, no. 1 (2022). http://dx.doi.org/10.1186/s12915-022-01385-1.

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Abstract Background Chromatin-modifying proteins are key players in the regulation of development and cell differentiation in animals. Most chromatin modifiers, however, predate the evolution of animal multicellularity, and how they gained new functions and became integrated into the regulatory networks underlying development is unclear. One way this may occur is the evolution of new scaffolding proteins that integrate multiple chromatin regulators into larger complexes that facilitate coordinated deposition or removal of different chromatin modifications. We test this hypothesis by analyzing

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Zeng, Cheng, Jiwei Chen, Emmalee W. Cooke, et al. "Demethylase-independent roles of LSD1 in regulating enhancers and cell fate transition." Nature Communications 14, no. 1 (2023). http://dx.doi.org/10.1038/s41467-023-40606-1.

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AbstractThe major enhancer regulator lysine-specific histone demethylase 1A (LSD1) is required for mammalian embryogenesis and is implicated in human congenital diseases and multiple types of cancer; however, the underlying mechanisms remain enigmatic. Here, we dissect the role of LSD1 and its demethylase activity in gene regulation and cell fate transition. Surprisingly, the catalytic inactivation of LSD1 has a mild impact on gene expression and cellular differentiation whereas the loss of LSD1 protein de-represses enhancers globally and impairs cell fate transition. LSD1 deletion increases H

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Chen, Zhuoyao, Gamma Chi, Timea Balo, et al. "Structural mimicry of UM171 and neomorphic cancer mutants co-opts E3 ligase KBTBD4 for HDAC1/2 recruitment." Nature Communications 16, no. 1 (2025). https://doi.org/10.1038/s41467-025-58350-z.

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Abstract Neomorphic mutations and drugs can elicit unanticipated effects that require mechanistic understanding to inform clinical practice. Recurrent indel mutations in the Kelch domain of the KBTBD4 E3 ligase rewire epigenetic programs for stemness in medulloblastoma by recruiting LSD1-CoREST-HDAC1/2 complexes as neo-substrates for ubiquitination and degradation. UM171, an investigational drug for haematopoietic stem cell transplantation, was found to degrade LSD1-CoREST-HDAC1/2 complexes in a wild-type KBTBD4-dependent manner, suggesting a potential common mode of action. Here, we identify

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Wu, Mingxuan, Dawn Hayward, Jay H. Kalin, Yun Song, John WR Schwabe, and Philip A. Cole. "Lysine-14 acetylation of histone H3 in chromatin confers resistance to the deacetylase and demethylase activities of an epigenetic silencing complex." eLife 7 (June 5, 2018). http://dx.doi.org/10.7554/elife.37231.

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The core CoREST complex (LHC) contains histone deacetylase HDAC1 and histone demethylase LSD1 held together by the scaffold protein CoREST. Here, we analyze the purified LHC with modified peptide and reconstituted semisynthetic mononucleosome substrates. LHC demethylase activity toward methyl-Lys4 in histone H3 is strongly inhibited by H3 Lys14 acetylation, and this appears to be an intrinsic property of the LSD1 subunit. Moreover, the deacetylase selectivity of LHC unexpectedly shows a marked preference for H3 acetyl-Lys9 versus acetyl-Lys14 in nucleosome substrates but this selectivity is lo

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