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Relevant bibliographies by topics / DNA methyltransferase (DNMT) inhibitor

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Academic literature on the topic 'DNA methyltransferase (DNMT) inhibitor'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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Journal articles on the topic "DNA methyltransferase (DNMT) inhibitor"

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Laranjeira, Angelo B. A., Dat Nguyen, Lorraine C. Pelosof, James H. Doroshow, and Sherry X. Yang. "Upregulation of TET2 and Resistance to DNA Methyltransferase (DNMT) Inhibitors in DNMT1-Deleted Cancer Cells." Diseases 12, no. 7 (2024): 163. http://dx.doi.org/10.3390/diseases12070163.

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Background: Ten-eleven-translocation (TET) 2 is a member of the TET family of proteins (TET1-3). DNMT1 gene deletion confers resistance to DNA methyltransferase (DNMT) inhibitors in colorectal, breast, and ovarian cancer cells. Currently, the effect of DNMT1 gene status on TET2 phenotype following DNMT inhibitor treatment is unclear in human malignancies. Methods: Human colorectal carcinoma HCT116 cells (DNMT+/+) and their isogenic DNMT1 knockout (DNMT1–/–) counterpart were treated with DNMT inhibitors. Expression of TET2 and tumor suppressor (p16ink4A and p15ink4B) proteins were examined by W

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Zimmermann, Nicole, Jürgen Zschocke, Tatjana Perisic, Shuang Yu, Florian Holsboer, and Theo Rein. "Antidepressants inhibit DNA methyltransferase 1 through reducing G9a levels." Biochemical Journal 448, no. 1 (2012): 93–102. http://dx.doi.org/10.1042/bj20120674.

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The discovery of epigenetic processes as possible pivotal regulatory mechanisms in psychiatric diseases raised the question of how psychoactive drugs may impact the epigenetic machinery. In the present study we set out to explore the specificity and the mode of action of the reported inhibitory effect of the TCA (tricyclic antidepressant) amitriptyline on DNMT (DNA methyltransferase) activity in primary astrocytes from the rat cortex. We found that the impact on DNMT was shared by another TCA, imipramine, and by paroxetine, but not by venlafaxine or the mood stabilizers carbamazepine and valpr

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Zhou, Zehao, Huan-Qiu Li, and Feng Liu. "DNA Methyltransferase Inhibitors and their Therapeutic Potential." Current Topics in Medicinal Chemistry 18, no. 28 (2019): 2448–57. http://dx.doi.org/10.2174/1568026619666181120150122.

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Aberrant DNA methylation at the 5-position of cytosine, catalyzed by DNA methyltransferases (DNMTs), is associated with not only various cancers by silencing of tumor suppressor genes but also other diseases. The DNMTs, especially the DNMT1, DNMT3A and DNMT3B, are often overexpressed in various cancer tissues and cell lines. DNMTs are important epigenetic targets for drug development since the DNA methylation is reversible. This review summarizes an array of nucleoside and non-nucleoside inhibitors of DNMTs, as well as their biological activities. Among these inhibitors, the nucleoside analogu

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Laranjeira, Angelo B., Dat Nguyen, Lorraine C. Pelosof, James H. Doroshow, and Sherry X. Yang. "Abstract 5881: Upregulation of TET2 expression by DNA methyltransferase (DNMT) inhibitors is associated with resistance in DNMT1 knockout colorectal cancer cells." Cancer Research 84, no. 6_Supplement (2024): 5881. http://dx.doi.org/10.1158/1538-7445.am2024-5881.

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Abstract Ten-eleven-translocation 2 (TET2) is a member of the TET family proteins (TET1-3) that convert 5-methylcytosine to 5-hydroxymethylcytosine (5-hmC) in DNA and causes site-specific DNA demethylation. The effects of DNMT1 on TET2 phenotype following DNMT inhibitor treatment is unclear in human cancer. In colorectal cancer HCT116 cells with DNMT1 gene intact (DNMT1+/+) and deletion (DNMT1−/−) status, we found that TET2 expression was robustly increased in DNMT1−/− cells after treatment with 0.5 µM and 5 µM decitabine for 72 h, 96 h, and 120 h. The augmentation in TET2 expression was accom

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Hupkes, Marlinda, Rita Azevedo, Hans Jansen, Everardus J. van Zoelen, and Koen J. Dechering. "Identification of Novel Bacterial M.SssI DNA Methyltransferase Inhibitors." Journal of Biomolecular Screening 18, no. 3 (2012): 348–55. http://dx.doi.org/10.1177/1087057112465009.

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DNA methylation is an important epigenetic regulator of gene expression. Abnormalities in DNA methylation patterns have been associated with various developmental and proliferative diseases, particularly cancer. Targeting DNA methyltransferases (DNMTs) represents a promising strategy for the treatment of such diseases. Current DNMT inhibitors suffer important drawbacks with respect to their efficacy, specificity, and toxicity. In this study, we have set up a robust in vitro bacterial M.SssI DNMT activity assay to systematically screen a collection of 26 240 compounds that were predicted to com

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Kim, Dae Joong. "The Role of the DNA Methyltransferase Family and the Therapeutic Potential of DNMT Inhibitors in Tumor Treatment." Current Oncology 32, no. 2 (2025): 88. https://doi.org/10.3390/curroncol32020088.

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Members of the DNA methyltransferase (DNMT) family have been recognized as major epigenetic regulators of altered gene expression during tumor development. They establish and maintain DNA methylation of the CpG island of promoter and non-CpG region of the genome. The abnormal methylation status of tumor suppressor genes (TSGs) has been associated with tumorigenesis, leading to genomic instability, improper gene silence, and immune evasion. DNMT1 helps preserve methylation patterns during DNA replication, whereas the DNMT3 family is responsible for de novo methylation, creating new methylation

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Prado-Romero, Diana L., Fernanda I. Saldívar-González, Iván López-Mata, et al. "De Novo Design of Inhibitors of DNA Methyltransferase 1: A Critical Comparison of Ligand- and Structure-Based Approaches." Biomolecules 14, no. 7 (2024): 775. http://dx.doi.org/10.3390/biom14070775.

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Designing and developing inhibitors against the epigenetic target DNA methyltransferase (DNMT) is an attractive strategy in epigenetic drug discovery. DNMT1 is one of the epigenetic enzymes with significant clinical relevance. Structure-based de novo design is a drug discovery strategy that was used in combination with similarity searching to identify a novel DNMT inhibitor with a novel chemical scaffold and warrants further exploration. This study aimed to continue exploring the potential of de novo design to build epigenetic-focused libraries targeted toward DNMT1. Herein, we report the resu

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Lakshmikuttyamma, Ashakumary, Stuart Scott, C. Ronald Geyer, and John F. DeCoteau. "Decreased Expression of the Histone Methyltransferase SUV39H1 in AML Cells Reactivates Hypermethylated Tumor Suppressor p15INK4B in the Absence of Promoter Demethylation." Blood 110, no. 11 (2007): 4150. http://dx.doi.org/10.1182/blood.v110.11.4150.4150.

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Abstract Re-expression of hypermethylated tumor suppressor genes using epigenetic modifiers, such as DNA methyltransferase (DNMT) and histone deacetylase (HDAC) inhibitors, occurs by a mechanism whereby promoter demethylation is the dominant event. In support of this model, we found that the DNMT inhibitor 5-Aza-2-deoxycytidine (decitabine) induces expression of the tumor suppressor gene p15INK4B (p15) in AML cells with hypermethylated p15 promoters. Re-expression of p15 by decitabine is associated with decreases in p15 promoter methylation and histone H3 lysine 9 (H3K9) methylation and increa

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Bhaskarawilaputraka, Igustingurah Raka, Azminah Azminah, Linda Erlina, Rezi Riadhi Syahdi, and Arry Yanuar. "VIRTUAL SCREENING OF INDONESIAN HERBAL DATABASE FOR DNA METHYLTRANSFERASE INHIBITORS." Asian Journal of Pharmaceutical and Clinical Research 10, no. 17 (2017): 153. http://dx.doi.org/10.22159/ajpcr.2017.v10s5.23120.

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Objective: DNA hypermethylation is an abnormal epigenetic process catalyzed by DNA methyltransferase 1 (DNMT1). It is also one of the factors that cause non-communicable diseases such as cancer, diabetes, and other metabolic diseases. DNA hypermethylation can be reversed by suppressing DNMT1 activity using a DNMT inhibitor. This study was conducted to seek out inhibitor candidates among natural products.Methods: The search for potential inhibitors was conducted through a virtual screening of the Indonesian Herbal Database using AutoDockVina as docking software. Twenty-five compounds known for

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Juárez-Mercado, K. Eurídice, Fernando D. Prieto-Martínez, Norberto Sánchez-Cruz, Andrea Peña-Castillo, Diego Prada-Gracia, and José L. Medina-Franco. "Expanding the Structural Diversity of DNA Methyltransferase Inhibitors." Pharmaceuticals 14, no. 1 (2020): 17. http://dx.doi.org/10.3390/ph14010017.

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Inhibitors of DNA methyltransferases (DNMTs) are attractive compounds for epigenetic drug discovery. They are also chemical tools to understand the biochemistry of epigenetic processes. Herein, we report five distinct inhibitors of DNMT1 characterized in enzymatic inhibition assays that did not show activity with DNMT3B. It was concluded that the dietary component theaflavin is an inhibitor of DNMT1. Two additional novel inhibitors of DNMT1 are the approved drugs glyburide and panobinostat. The DNMT1 enzymatic inhibitory activity of panobinostat, a known pan inhibitor of histone deacetylases,

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Dissertations / Theses on the topic "DNA methyltransferase (DNMT) inhibitor"

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BAIAMONTE, Concetta. "Reactivation of SNURF-SNRPN gene by DNA Methyltransferase inhibitors in a Prader-Willi lymphoblastoid cell line." Doctoral thesis, Università degli Studi di Palermo, 2014. http://hdl.handle.net/10447/91240.

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Pechalrieu, Dany. "Des inhibiteurs de méthyltransférases de l'ADN au développement de sondes chimiques pour l'identification de modulateurs épigénétiques dérégulés dans les cancers." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30185.

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Les méthyltransférases de l'ADN (DNMT) catalysent la méthylation de l'ADN, l'une des marques épigénétiques les plus étudiées. Dans les cancers, on observe une hyperméthylation spécifique de promoteurs de gènes suppresseurs de tumeurs (GST) conduisant à leur extinction génique, ce qui participe au maintien et à la progression de tumeurs. A ce jour, les mécanismes responsables de cette hyperméthylation spécifique des promoteurs de GST dans les cancers sont indéterminés. Ces travaux de thèse sont consacrés à l'inhibition des DNMT dans les cancers afin de restaurer l'expression des GST mais égalem

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Erdmann, Alexandre. "Conception, synthèse et caractérisation de nouveaux inhibiteurs de méthyltranférases d'ADN à visée anticancéreuse." Thesis, Toulouse 3, 2015. http://www.theses.fr/2015TOU30270.

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Le domaine de l'épigénétique couvre l'ensemble des phénomènes héritables et transmissibles qui interviennent dans l'expression du génome sans modifier la séquence nucléotidique. L'information épigénétique est régulée par les modifications de la chromatine impliquant les histones et l'ADN. La méthylation de l'ADN est un phénomène réversible jouant un rôle crucial dans l'expression des gènes puisque la méthylation des promoteurs de gènes empêche leur transcription. La modulation aberrante de cette marque épigénétique est associée à diverses pathologies telles que le cancer. Cette méthylation éta

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Kuch, David. "Synthese und Charakterisierung neuartiger Inhibitoren für die humane DNA Methyltransferase DNMT1 /." München : Dr. Hut Verlag, 2009. http://edoc.ub.uni-muenchen.de/9490/.

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Kuch, David. "Synthese und Charakterisierung neuartiger Inhibitoren für die humane DNA Methyltransferase DNMT1." Diss., lmu, 2008. http://nbn-resolving.de/urn:nbn:de:bvb:19-94905.

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Elkovich, Andrea J. "The DNA methyltransferase inhibitor, guadecitabine, targets tumor-induced myelopoiesis and recovers T cell activity to slow tumor growth." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5792.

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Myeloid Derived Suppressor Cells (MDSC) represent a significant hurdle to cancer immunotherapy because they dampen anti-tumor cytotoxic T cell responses. Previous studies have reported on the myelo-depletive effects of certain chemotherapies. Using guadecitabine, a next-generation DNA methyltransferase inhibitor (DNMTi), we observed significantly reduced tumor burden in the 4T1 murine mammary carcinoma model. Guadecitabine treatment prevents excessive tumor-induced myeloid proliferation and systemic accumulation, and skews remaining MDSCs toward a beneficial antigen-presenting phenotype. Toget

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Benson, Jennifer. "Effect of the DNA Methylation Inhibitor 5-aza-2'-Deoxycytidine on the Virulence of the Soybean Pathogen Phytophthora Sojae." Bowling Green State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1342052698.

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SHIH, CHIH-CHIN, and 施志勤. "Effects and Mechanisms of DNA Methyltransferase 1 (DNMT1) Inhibitor Procainamide on Endotoxemic Rats." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/5cpk7c.

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博士<br>國防醫學院<br>醫學科學研究所<br>105<br>Excessive inflammatory and oxidative stress lead to circulatory failure, multiple organ dysfunction, and high mortality in patients with sepsis. Microbial infection-induced DNA hypermethylation is associated with the augmentation of inflammation and oxidative stress. The antiarrhythmic drug procainamide is a non-nucleoside inhibitor of DNA methyltransferase 1 (DNMT1) used to alleviate DNA hypermethylation. Therefore, we evaluated effects of procainamide on the development of circulatory failure and multiple organ dysfunction in rats with endotoxic shock. Male W

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Priyadarshini, D. Indira. "Role Of DNA Methyltransferase 1, “DNMT 1” In Human Cancer." Thesis, 2011. http://ethesis.nitrkl.ac.in/2387/1/INDU_FINAL.pdf.

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Changes in methylation of promoter or first exon may mimic the effect of mutations of various tumor suppressor genes (TSGs) or proto- oncogene. Repression of various genes during malignant transformation is due to CpG island hypermethylation and chromatin remodeling. Transcriptional-silencing is due to the Hypermethylation of promoter of various TSGs. However, hypomethylation of regulatory DNA sequences activates transcription of proto-oncogene, retrotransposons, as well as genes encoding proteins involved in genomic instability and malignant cell metastasis. The methylation of genomic DNA in

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Kuch, David [Verfasser]. "Synthese und Charakterisierung neuartiger Inhibitoren für die humane DNA-Methyltransferase DNMT1 / David Kuch." 2008. http://d-nb.info/993090370/34.

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Books on the topic "DNA methyltransferase (DNMT) inhibitor"

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Trus, Michael. Altering retinoid sensitivity in acute myeloblastic leukemia cells by treatment with the histone deacetylase inhibitor, valproic acid, and the inhibitor of DNA methyltransferase activity, 5-aza-2'-deoxycytidine. 2006.

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Book chapters on the topic "DNA methyltransferase (DNMT) inhibitor"

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Arnemann, J. "DNA-Methyltransferase (DNMT)." In Springer Reference Medizin. Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_3463.

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Arnemann, J. "DNA-Methyltransferase (DNMT)." In Lexikon der Medizinischen Laboratoriumsdiagnostik. Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-662-49054-9_3463-1.

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Van Camp, Jennifer A. "Decitabine (Dacogen): A DNA Methyltransferase Inhibitor for Cancer." In Modern Drug Synthesis. John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470768594.ch4.

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Lübbert, Michael, Michael Daskalakis, Philipp N. Sander, and Andrea Kündgen. "Azanucleoside DNA Methyltransferase Inhibitor Drugs: Update on Clinical Applications in Myelodysplastic Syndromes and Acute Myeloid Leukemia." In Epigenetics - A Different Way of Looking at Genetics. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27186-6_10.

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Nikolić, Patrik, Vedran Miletić, Ivica Odorcić, and Željko M. Svedružić. "In Silico Optimization of the First DNA-Independent Mechanism-Based Inhibitor of Mammalian DNA Methyltransferase DNMT1." In Epi-Informatics. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-802808-7.00005-8.

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"DNA Methyltransferase (DNMT)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics. Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_4670.

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"DNA Methyltransferase Inhibitor Therapy in the Treatment of Myelodysplastic Syndromes." In Myelodysplastic Syndromes. CRC Press, 2008. http://dx.doi.org/10.3109/9781420074406-24.

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Conference papers on the topic "DNA methyltransferase (DNMT) inhibitor"

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Laranjeira, Angelo B., Dat Nguyen, Erich Huang, James H. Doroshow, and Sherry X. Yang. "Abstract 5081: Disruption of DNA methyltransferase (DNMT) 1 confers resistance to DNMT inhibitors in human colorectal cancer cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5081.

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Cheishvili, David, and Moshe Szyf. "Abstract 4349: Adverse & anticancer activities of 5-azaCdR & DNA methyltransferase (DNMT) isoform specific inhibitors: therapeutic implications." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4349.

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Yang, Sherry X., Dat Nguyen, Larry Rubinstein, Alice P. Chen, and James H. Doroshow. "Abstract B12: DNA methyltransferase 3A expression in cancer cells following treatment with DNMT inhibitors and in human solid tumors." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; November 5-9, 2015; Boston, MA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1535-7163.targ-15-b12.

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Zhang, Qiang, Brian Helfand, Xiao Lin та ін. "Abstract 4038: Human prostate cancer invasion could be suppressed by 5-Aza-2′-deoxycytidine which can inhibit the TGF-β induced DNA methyltransferase (DNMT)". У Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4038.

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Katz, Tiffany A., Shauna N. Vasilatos, Steffi Oesterreich, Uma Chandran, Nancy E. Davidson, and Yi Huang. "Abstract 1052: Synergy between inhibition of novel histone demethylase (LSD2) and DNA methyltransferase (DNMT) and histone deacetylase (HDAC) in modulating gene expression and inhibiting growth in human breast cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1052.

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Nguyen, Dat, Melinda Hollingshead, Larry Rubinstein, James Doroshow, and Sherry X. Yang. "Abstract 4722: Selective inhibition of DNA methyltransferases and efficacy of novel DNMT inhibitors in leukemia xenografts." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4722.

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Martínez Fernández, Liliam, and Jose Luis Medina Franco. "Identification of novel DNA Methyltransferase 1 (DNMT1) inhibitors from focused databases." In 7th International Electronic Conference on Medicinal Chemistry. MDPI, 2021. http://dx.doi.org/10.3390/ecmc2021-11570.

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Zhang, Qiang, Lin Chen, Brian Helfand, Thomas Jang, Yinglu Guo, and Chung Lee. "Abstract 3185: Expression of DNA methyltransferase (DNMT) induced by transforming growth factor-ß (TGF-ß) promotes progress of prostate cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3185.

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Bai, Yuchen Vincent, John Whitaker, Emanuele Palescandolo, et al. "Abstract 5371: Effect of DNA methyltransferase inhibitor 5-azacitidine on 3D chromatin structure measured by Hi-C." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5371.

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Liu, Minmin, Toshinori Hinoue, Wanding Zhou, et al. "Abstract 779: Integrative analysis reveals therapeutic targets to the DNA methyltransferase inhibitor SGI-110 in hepatocellular carcinoma." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-779.

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