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

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Published: 3 June 2025

Last updated: 31 July 2025

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1

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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Zwergel, Clemens, Rossella Fioravanti, Giulia Stazi, et al. "Novel Quinoline Compounds Active in Cancer Cells through Coupled DNA Methyltransferase Inhibition and Degradation." Cancers 12, no. 2 (2020): 447. http://dx.doi.org/10.3390/cancers12020447.

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DNA methyltransferases (DNMTs) play a relevant role in epigenetic control of cancer cell survival and proliferation. Since only two DNMT inhibitors (azacitidine and decitabine) have been approved to date for the treatment of hematological malignancies, the development of novel potent and specific inhibitors is urgent. Here we describe the design, synthesis, and biological evaluation of a new series of compounds acting at the same time as DNMTs (mainly DNMT3A) inhibitors and degraders. Tested against leukemic and solid cancer cell lines, 2a–c and 4a–c (the last only for leukemias) displayed up

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Yang, Wei, Jingyuan Zhuang, Chen Li, Chen Bai, and Guijuan Cheng. "Insights into the Inhibitory Mechanisms of the Covalent Drugs for DNMT3A." International Journal of Molecular Sciences 24, no. 16 (2023): 12652. http://dx.doi.org/10.3390/ijms241612652.

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The perturbations of DNA methyltransferase 3 alpha (DNMT3A) may cause uncontrolled gene expression, resulting in cancers and tumors. The DNMT inhibitors Azacytidine (AZA) and Zebularine (ZEB) inhibit the DNMT family with no specificities, and consequently would bring side effects during the treatment. Therefore, it is vital to understand the inhibitory mechanisms in DNMT3A to inform the new inhibitor design for DNMTs. Herein, we carried out molecular dynamics (MD) and quantum mechanics/molecular mechanics (QM/MM) simulations to investigate the inhibitory mechanisms of the AZA and ZEB. The resu

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Kritsi, Eftichia, Paris Christodoulou, Thalia Tsiaka, Panagiotis Georgiadis, and Maria Zervou. "A Computational Approach for the Discovery of Novel DNA Methyltransferase Inhibitors." Current Issues in Molecular Biology 46, no. 4 (2024): 3394–407. http://dx.doi.org/10.3390/cimb46040213.

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Nowadays, the explosion of knowledge in the field of epigenetics has revealed new pathways toward the treatment of multifactorial diseases, rendering the key players of the epigenetic machinery the focus of today’s pharmaceutical landscape. Among epigenetic enzymes, DNA methyltransferases (DNMTs) are first studied as inhibition targets for cancer treatment. The increasing clinical interest in DNMTs has led to advanced experimental and computational strategies in the search for novel DNMT inhibitors. Considering the importance of epigenetic targets as a novel and promising pharmaceutical trend,

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Ranju, Kunwor, Su Yanrong, Santucci-Pereira Julia, and Russo Jose. "Present status of epigenetic drugs in cancer treatment." Biohelikon 3, no. 1 (2015): 1–15. https://doi.org/10.5281/zenodo.814341.

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Epigenetic changes such as promoter specific DNA hypermethylation and histone deacetylation cause tumor suppressor genes to become transcriptionally silent and contribute to malignant transformation. DNA methyltransferase (DNMT) and histone deacetylase (HDAC) inhibitors can reactivate silenced genes, block cell cycle and induce cell apoptosis which provides rationale for their use in cancer treatment. DNMT and HDAC inhibitors have therefore emerged as an effective strategy against cancer. Epigenetic modifications have a key role in the pathophysiology of many cancers such as myelodysplastic sy

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Lamothe, J., S. Khurana, S. Tharmalingam, et al. "The Role of DNMT and HDACs in the Fetal Programming of Hypertension by Glucocorticoids." Oxidative Medicine and Cellular Longevity 2020 (March 30, 2020): 1–17. http://dx.doi.org/10.1155/2020/5751768.

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The causes of hypertension are complex and involve both genetic and environmental factors. Environment changes during fetal development have been linked to adult diseases including hypertension. Studies show that timed in utero exposure to the synthetic glucocorticoid (GC) dexamethasone (Dex) results in the development of hypertension in adult rats. Evidence suggests that in utero stress can alter patterns of gene expression, possibly a result of alterations in the topology of the genome by epigenetic markers such as DNA methyltransferases (DNMTs) and histone deacetylases (HDACs). The objectiv

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Laranjeira, Angelo B., Melinda Hollingshead, Dat Nguyen, et al. "Abstract LB192: Demethylation, DNA damage and antitumor activity of DNA methyltransferase inhibitors in models with intact and disrupted DNMT1 gene." Cancer Research 82, no. 12_Supplement (2022): LB192. http://dx.doi.org/10.1158/1538-7445.am2022-lb192.

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Abstract DNA methyltransferase (DNMT) 1 is an enzyme responsible for maintaining DNA methylation pattern during DNA replication. However, its role on the methylation of tumor suppressor genes and DNA damage in relation to antitumor activity of DNMT inhibitors remains controversial. Here, we investigated the effects of DNMT inhibitors in human colorectal and breast cancer cell lines and animal models with intact (DNMT1+/+) and disrupted DNMT1 (DNMT1-/-) gene. Treatment with 5 µM of 4’-thio-5-aza-2’-deoxycytidine (aza-TdC), decitabine and azacytidine all inhibited DNMT1 expression and cell growt

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Wang, Liqing, Yujie Liu, Ulf H. Beier, et al. "Foxp3+ T-regulatory cells require DNA methyltransferase 1 expression to prevent development of lethal autoimmunity." Blood 121, no. 18 (2013): 3631–39. http://dx.doi.org/10.1182/blood-2012-08-451765.

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Key Points Foxp3 expression is increased by DNMT inhibitors and may have potential utility in efforts to develop Foxp3+ Tregs for cellular therapy. Dnmt1 deletion impairs Treg function and results in lethal autoimmunity, such that use of Dnmt inhibitors may warrant careful consideration.

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Vernier, Mathieu, Shawn McGuirk, Catherine R. Dufour та ін. "Inhibition of DNMT1 and ERRα crosstalk suppresses breast cancer via derepression of IRF4". Oncogene 39, № 41 (2020): 6406–20. http://dx.doi.org/10.1038/s41388-020-01438-1.

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Abstract DNA methylation is implicated in the acquisition of malignant phenotypes, and the use of epigenetic modulating drugs is a promising anti-cancer therapeutic strategy. 5-aza-2’deoxycytidine (decitabine, 5-azadC) is an FDA-approved DNA methyltransferase (DNMT) inhibitor with proven effectiveness against hematological malignancies and more recently triple-negative breast cancer (BC). Herein, genetic or pharmacological studies uncovered a hitherto unknown feedforward molecular link between DNMT1 and the estrogen related receptor α (ERRα), a key transcriptional regulator of cellular metabol

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Hopfer, Olaf J., Martina Komor, Ina S. Koehler, et al. "Expression of DNMT Isoforms Is Differentially Associated with Aberrant Promotor Methylation in MDS Hematopoietic Progenitor Cells during Lineage Specific Differentiation." Blood 108, no. 11 (2006): 2628. http://dx.doi.org/10.1182/blood.v108.11.2628.2628.

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Abstract Recent findings suggest that in myelodysplastic syndrome (MDS) several key regulatory genes are affected by aberrant promotor methylation. To explore the molecular basis of this impairment we have generated an in vitro model of MDS lineage-specific hematopoietic differentiation by culturing CD34+ cells from healthy donors (n=7) and MDS patients (low risk: RA/n=6, RARS/n=3; high risk: RAEB/n=4, RAEB-T/n=2) with EPO, TPO and GCSF. Cell harvest was at days 0, 4, 7 and 11. Promotor methylation analysis of key genes involved in the control of apoptosis (p73, survivin, DAPK), DNA-repair (hM

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Huber, Anne, Christine Dijkstra, Yuba Bhandari, et al. "Abstract A008: DNA methyltransferase 3A promotes inflammation-associated gastric cancer growth and presents a therapy target for gastric cancer." Cancer Research 82, no. 23_Supplement_2 (2022): A008. http://dx.doi.org/10.1158/1538-7445.cancepi22-a008.

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Abstract Gastric cancer (GC) remains the third leading cause of cancer-related death worldwide. While inflammation is a well-established driver of gastric tumorigenesis, only a small subset of GC patients responds to immunotherapy. One proposed mechanism of immune escape is silencing tumor-antigen expression, and thereby avoiding immune recognition. DNA methyltransferases (DNMTs) are the enzymes responsible for DNA methylation and hence, for the epigenetic silencing of gene expression of tumor-antigens and other immune-related molecules. Interestingly, they are often overexpressed in solid tum

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Borutinskaite, Veronika, Justina Bauraite-Akatova, and Ruta Navakauskiene. "Anti-leukemic activity of DNA methyltransferase inhibitor procaine targeted on human leukaemia cells." Open Life Sciences 11, no. 1 (2016): 322–30. http://dx.doi.org/10.1515/biol-2016-0044.

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AbstractChromatin remodeling in DNA is fundamental to gene expression, DNA replication and repair processes. Methylation of promoter regions of tumor-suppressor genes and histone deacetylation leads to gene silencing and transcriptionally repressive chromatin. For the past few decades DNA methylation agents became very attractive as the targets for cancer therapy. The purpose of this work was to examine the effects of DNMT inhibitor procaine on growth inhibition, apoptosis and differentiation of human leukaemia cells. The changes in expression of genes, proteins and histone modifications cause

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Fiskus, Warren, Pace Johnston, Rajeshree Joshi, et al. "Anti-AML Activity of Combined Epigenetic Therapy with Novel DNMT1 Inhibitors SGI-110 or SGI-1036 and Histone Deacetylase Inhibitor Panobinostat." Blood 112, no. 11 (2008): 3355. http://dx.doi.org/10.1182/blood.v112.11.3355.3355.

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Abstract Lysine specific histone methylation and deacetylation and DNA hypermethylation are involved in the epigenetic silencing of tumor suppressor genes (TSG), e.g., p15 and p16. DNA methyltransferase (DNMT) inhibitors 5-azacytidine and 5-aza-2’-deoxycytidine demethylate the CpG dinucleotide islands in or near gene promoters, leading to derepression of TSGs in AML. SGI-110 (S110) (Cancer Res.2007; 67:6400) and SGI-1036 (SuperGen, Inc.) are novel, DNMT inhibitors, which also deplete DNMT1 levels. SGI-110 is a dinucleotide containing 5-aza-2’-deoxycytidine and SGI-1036 is a non-nucleoside hete

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Wanga, Xin-zhi, Jia-li Gu, Ming Gao, et al. "Peperomin E Induces Promoter Hypomethylation of Metastatic-Suppressor Genes and Attenuates Metastasis in Poorly Differentiated Gastric Cancer." Cellular Physiology and Biochemistry 50, no. 6 (2018): 2341–64. http://dx.doi.org/10.1159/000495096.

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Background/Aims: Peperomin E (PepE), a natural secolignan isolated from the whole plant of Peperomia dindygulensis, has been reported by ourselves and others to display potent anti-cancer effects in many types cancer cells, especially gastric cancer. However, the effects of PepE on the metastasis of poorly-differentiated gastric cancer cells and the underlying molecular mechanisms have not been well elucidated. Methods: We evaluated PepE effects on gastric cancer cell invasion and migration in vitro via wound healing and transwell assays and those on growth and metastasis in vivo using an orth

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Hooi, Lissa, Vivien Koh, Dexter Kai Hao Thng, et al. "Abstract P43: Optimization of DNA Methyltransferase Inhibitors-based Combination to Target the Epigenome of Gastric Cancer." Cancer Research 84, no. 8_Supplement (2024): P43. http://dx.doi.org/10.1158/1538-7445.fcs2023-p43.

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Abstract Aberrant DNA methylation is one of the critical epigenetic modifications that has become a widespread phenotype in solid tumours. Similar to haematological malignancies, many studies have shown that the DNA methylation landscape of solid tumours exhibits a pattern of either hypermethylation of the promoter regions of tumour-suppressive genes in advanced cancer or global hypomethylation in the early stages of carcinogenesis. Additionally, dysregulated DNA methylation also seems to remodel the tumour microenvironment and affect immune cells' response towards immune checkpoint inhibitors

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Zhu, Huolan, Xiang Wang, Xuyang Meng, et al. "Selenium Supplementation Improved Cardiac Functions by Suppressing DNMT2-Mediated GPX1 Promoter DNA Methylation in AGE-Induced Heart Failure." Oxidative Medicine and Cellular Longevity 2022 (April 6, 2022): 1–12. http://dx.doi.org/10.1155/2022/5402997.

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Objective. Advanced glycation end products (AGEs) are featured metabolites associated with diabetic cardiomyopathy which is characterized by heart failure caused by myocyte apoptosis. Selenium was proved cardioprotective. This study was aimed at investigating the therapeutic effects and underlying mechanisms of selenium supplementation on AGE-induced heart failure. Methods. Rats and primary myocytes were exposed to AGEs. Selenium supplementation was administrated. Cardiac functions and myocyte apoptosis were evaluated. Oxidative stress was assessed by total antioxidant capacity (TAC), reactive

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Mitsuhashi, Risa, Kiyoshi Sato, and Hiroyoshi Kawakami. "Novel Epigenetics Control (EpC) Nanocarrier for Cancer Therapy Through Dual-Targeting Approach to DNA Methyltransferase and Ten-Eleven Translocation Enzymes." Epigenomes 9, no. 1 (2025): 6. https://doi.org/10.3390/epigenomes9010006.

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Background/Objectives: Aberrant hypermethylation in the promoter regions of tumor suppressor genes facilitates the pathogenesis and progression of cancer. Therefore, inhibitors targeting DNA methyltransferase (DNMT) have been tested in clinical studies. However, the current monotherapy of DNMT inhibitors shows limited efficacy. Furthermore, the mechanism of action of DNMT inhibitors is DNA replication-dependent. To address these limitations, we developed a novel core–shell-type “epigenetics control (EpC) nanocarrier” that encapsulated decitabine (5-aza-dC) in the PLGA core nanoparticle and hyb

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Wang, Chenyin, Lijuan Lei, Yang Xu, et al. "Trichostatin C Synergistically Interacts with DNMT Inhibitor to Induce Antineoplastic Effect via Inhibition of Axl in Bladder and Lung Cancer Cells." Pharmaceuticals 17, no. 4 (2024): 425. http://dx.doi.org/10.3390/ph17040425.

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Aberrant epigenetic modifications are fundamental contributors to the pathogenesis of various cancers. Consequently, targeting these aberrations with small molecules, such as histone deacetylase (HDAC) inhibitors and DNA methyltransferase (DNMT) inhibitors, presents a viable strategy for cancer therapy. The objective of this study is to assess the anti-cancer efficacy of trichostatin C (TSC), an analogue of trichostatin A sourced from the fermentation of Streptomyces sp. CPCC 203909. Our investigations reveal that TSC demonstrates potent activity against both human lung cancer and urothelial b

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Fukui, Taro, Kuniyasu Soda, Koichi Takao, and Toshiki Rikiyama. "Extracellular Spermine Activates DNA Methyltransferase 3A and 3B." International Journal of Molecular Sciences 20, no. 5 (2019): 1254. http://dx.doi.org/10.3390/ijms20051254.

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We first demonstrated that long-term increased polyamine (spermine, spermidine, putrescine) intake elevated blood spermine levels in mice and humans, and lifelong consumption of polyamine-rich chow inhibited aging-associated increase in aberrant DNA methylation, inhibited aging-associated pathological changes, and extend lifespan of mouse. Because gene methylation status is closely associated with aging-associated conditions and polyamine metabolism is closely associated with regulation of gene methylation, we investigated the effects of extracellular spermine supplementation on substrate conc

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Gore, Steven D. "New Ways to Use DNA Methyltransferase Inhibitors for the Treatment of Myelodysplastic Syndrome." Hematology 2011, no. 1 (2011): 550–55. http://dx.doi.org/10.1182/asheducation-2011.1.550.

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AbstractOngoing analysis of the seminal AZA-001 study has taught many important lessons in the use of DNA methyltransferase (DNMT) inhibitors. The data emphasize the importance of patience in the use of these drugs, with several cycles required for the manifestations of hematologic responses. Improved survival in patients with high-risk myelodysplastic syndrome (MDS) treated with azacitidine extends to patients with any International Working Group–defined hematologic response; however, the benefit to patients with stable disease is less clear. A great deal remains to be learned about the optim

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Weisenberger, Daniel J., Mihaela Velicescu, Jonathan C. Cheng, Felicidad A. Gonzales, Gangning Liang, and Peter A. Jones. "Role of the DNA Methyltransferase Variant DNMT3b3 in DNA Methylation." Molecular Cancer Research 2, no. 1 (2004): 62–72. http://dx.doi.org/10.1158/1541-7786.62.2.1.

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Abstract Several alternatively spliced variants of DNA methyltransferase (DNMT) 3b have been described. Here, we identified new murine Dnmt3b mRNA isoforms and found that mouse embryonic stem (ES) cells expressed only Dnmt3b transcripts that contained exons 10 and 11, whereas the Dnmt3b transcripts in somatic cells lacked these exons, suggesting that this region is important for embryonic development. DNMT3b2 and 3b3 were the major isoforms expressed in human cell lines and the mRNA levels of these isoforms closely correlated with their protein levels. Although DNMT3b3 may be catalytically ina

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Shaknovich, Rita, Leandro Cerchietti, Lucas Tsikitas, et al. "DNA methyltransferase 1 and DNA methylation patterning contribute to germinal center B-cell differentiation." Blood 118, no. 13 (2011): 3559–69. http://dx.doi.org/10.1182/blood-2011-06-357996.

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Abstract The phenotype of germinal center (GC) B cells includes the unique ability to tolerate rapid proliferation and the mutagenic actions of activation induced cytosine deaminase (AICDA). Given the importance of epigenetic patterning in determining cellular phenotypes, we examined DNA methylation and the role of DNA methyltransferases in the formation of GCs. DNA methylation profiling revealed a marked shift in DNA methylation patterning in GC B cells versus resting/naive B cells. This shift included significant differential methylation of 235 genes, with concordant inverse changes in gene

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Del Castillo Falconi, Victor M., Karla Torres-Arciga, Genaro Matus-Ortega, José Díaz-Chávez, and Luis A. Herrera. "DNA Methyltransferases: From Evolution to Clinical Applications." International Journal of Molecular Sciences 23, no. 16 (2022): 8994. http://dx.doi.org/10.3390/ijms23168994.

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DNA methylation is an epigenetic mark that living beings have used in different environments. The MTases family catalyzes DNA methylation. This process is conserved from archaea to eukaryotes, from fertilization to every stage of development, and from the early stages of cancer to metastasis. The family of DNMTs has been classified into DNMT1, DNMT2, and DNMT3. Each DNMT has been duplicated or deleted, having consequences on DNMT structure and cellular function, resulting in a conserved evolutionary reaction of DNA methylation. DNMTs are conserved in the five kingdoms of life: bacteria, protis

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Li, Y., H. D. Morgan, L. Ganeshan, and C. O'Neill. "124. DNA METHYLATION IN THE 2-CELL MOUSE EMBRYO IS THE RESULT OF DNMT ACTIVITY DURING DEVELOPMENT FROM THE ZYGOTE TO THE 2-CELL STAGE." Reproduction, Fertility and Development 21, no. 9 (2009): 43. http://dx.doi.org/10.1071/srb09abs124.

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In an accompanying abstract we show for the first time that global demethylation of both paternally- and maternally-derived genomes occurs prior to syngamy. It is commonly considered that new methylation of the genome does not commence until late in the preimplantation stage. Yet embryos during cleavage stage are known to show DNA methylation. This creates a paradox, if global demethylation occurs by the time of syngamy yet remethylation does not occur until the blastocysts stage, how can cleavage stage embryos possess methylated DNA. We examined this paradox. We examined DNA methylation in 2-

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Jamaluddin, S., Irene Chen, Fan Yang, et al. "Homocysteine Inhibits Cyclin A Promoter Methylation Via DNMT3 Inactivation in Human Endothelial Cells." Blood 108, no. 11 (2006): 1822. http://dx.doi.org/10.1182/blood.v108.11.1822.1822.

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Abstract Hyperhomocysteinemia is a significant and independent risk factor for cardiovascular disease. We reported previously that homocysteine (Hcy) inhibits endothelial cell (EC) growth by transcriptional inhibition of the cyclin A gene. This is associated with an increase in S-adenosylhomocysteine, a potent inhibitor of methyltransferase. We hypothesized that Hcy inhibits EC growth and cyclin A transcription via hypomethylation and studied the effect of Hcy on epigenetic regulation of the cyclin A gene in EC. We found that the levels of cyclin A mRNA were significantly suppressed by azacyti

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Mohan, Nila. "Nucleoside and Non-Nucleoside DNA Methyltransferase 1 Inhibitors in Epigenetic and Combination Therapies in Cancer: A Scoping Review." Undergraduate Research in Natural and Clinical Science and Technology (URNCST) Journal 9, no. 1 (2025): 1–8. https://doi.org/10.26685/urncst.641.

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DNA methylation is an epigenetic mechanism of gene silencing crucial to the regulation of gene expression in normal physiological events such as differentiation and X-inactivation. However, aberrant silencing of regulatory genes can contribute to oncogenic transformation, further perpetuated due to the heritability of these changes down the cell line. Though aberrant DNA methylation is implicated across cancer types, epigenetic therapy with DNA methyltransferase 1 (DNMT1) depleting drugs is only approved in the treatment of hematological cancers. This limitation is due to the drugs’ high toxic

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Kumari, L. R. L. S., and W. R. P. Wijesinghe. "Computer-aided drug design to discover DNMT inhibitors from phytochemicals." Ceylon Journal of Science 53, no. 2 (2024): 275–90. http://dx.doi.org/10.4038/cjs.v53i2.8262.

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Inhibitors of DNA methyltransferase (DNMTs) are now a major family of epigenetic targets with therapeutic interest. However, only two cytosine analogues 5-azacytosine (azacytidine) and 20-deoxy-5-azacytidine (decitabine), have been approved as the most cutting-edge medications for treating epigenetic cancer with some restrictions. In this context, computational methods that rely on quantitative structure-activity relationship (QSAR) play a crucial role allowing us to predict the biological activity of potential molecules based on the theoretically calculated physicochemical properties of these

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Steers, Garett J., Brianne R. O’Leary, Juan Du, et al. "Pharmacologic Ascorbate and DNMT Inhibitors Increase DUOX Expression and Peroxide-Mediated Toxicity in Pancreatic Cancer." Antioxidants 12, no. 9 (2023): 1683. http://dx.doi.org/10.3390/antiox12091683.

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Recent studies have demonstrated an important role for vitamin C in the epigenetic regulation of cancer-related genes via DNA demethylation by the ten-eleven translocation (TET) methylcytosine dioxygenase enzymes. DNA methyltransferase (DNMT) reverses this, increasing DNA methylation and decreasing gene expression. Dual oxidase (DUOX) enzymes produce hydrogen peroxide (H2O2) in normal pancreatic tissue but are silenced in pancreatic cancer (PDAC). Treatment of PDAC with pharmacologic ascorbate (P-AscH−, intravenous, high dose vitamin C) increases DUOX expression. We hypothesized that inhibitin

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Ureshino, Hiroshi, Tatsuro Watanabe, Yuki Kurahashi, et al. "OR21, a New Oral DNA Methyltransferase Inhibitor for Treatment of MDS and AML." Blood 132, Supplement 1 (2018): 5499. http://dx.doi.org/10.1182/blood-2018-99-112362.

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Abstract Myelodysplastic syndromes (MDS) is a clonal disorder caused by mutation in hematopoietic stem cells (HSCs), including several somatic mutations and aberrant DNA hypermethylation, which can induce silence of tumor-suppressor genes and lead to the pathogenesis and/or progression of MDS. Thus, reducing methylation with the aim of genes reestablishing the expression of silenced tumor-suppressor genes represents one promising approach for the treatment of MDS. Azacytidine (AZA) and/or decitabine (DAC), two DNA methyltransferase (DNMT) inhibitors currently available for the treatment of MDS

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Boosani, Chandra S., Palanikumar Gunasekar, Megan Block, et al. "Inhibition of DNA methyltransferase-1 instigates the expression of DNA methyltransferase-3a in angioplasty-induced restenosis." Canadian Journal of Physiology and Pharmacology 96, no. 10 (2018): 1030–39. http://dx.doi.org/10.1139/cjpp-2018-0111.

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Increased expression of DNA methyltransferase-1 (DNMT1) associates with the progression of many human diseases. Because DNMT1 induces cell proliferation, drugs that inhibit DNMT1 have been used to treat proliferative diseases. Because these drugs are nonspecific inhibitors of DNMT1, subsidiary events or the compensatory mechanisms that are activated in the absence of DNMT1 limit their therapeutic application. Here, we studied the molecular mechanisms that occur during angioplasty-induced restenosis and found that DNMT1 inhibition in both in vitro and in vivo approaches resulted in the inductio

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Neveu, Wendy A., Stephen T. Mills, Bashar S. Staitieh та Viranuj Sueblinvong. "TGF-β1 epigenetically modifies Thy-1 expression in primary lung fibroblasts". American Journal of Physiology-Cell Physiology 309, № 9 (2015): C616—C626. http://dx.doi.org/10.1152/ajpcell.00086.2015.

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Idiopathic pulmonary fibrosis is a progressive lung disease that increases in incidence with age. We identified a profibrotic lung phenotype in aging mice characterized by an increase in the number of fibroblasts lacking the expression of thymocyte differentiation antigen 1 (Thy-1) and an increase in transforming growth factor (TGF)-β1 expression. It has been shown that Thy-1 expression can be epigenetically modified. Lung fibroblasts (PLFs) were treated with TGF-β1 ± DNA methyltransferase (DNMT) inhibitor 5-aza-2′-deoxycytidine (5-AZA) and analyzed for Thy-1 gene and protein expression, DNMT

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Márquez-Sánchez, Ana Cristina, Alejandro Manzanares-Guzmán, Ramón Carriles-Jaimes, et al. "Nanoparticles loaded with the DNA methyltransferase inhibitor SGI-1027 decrease murine atherosclerosis and inflammation in cultured human macrophages." Exploration of Cardiology 2, no. 2 (2024): 49–66. http://dx.doi.org/10.37349/ec.2024.00021.

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Aim: The DNA of the atheroma is hypermethylated relative to adjacent healthy vascular tissue. A significant portion of hypermethylated loci in the atheroma DNA map to genes related to macrophage function. Reversing macrophage DNA methylation to physiological levels by targeting DNA methyltransferase (DNMT) activity may therefore slow atherogenesis. Here, the anti-inflammatory and anti-atherogenic activity of macrophage-targeted DNMT inhibitor SGI-1027 were tested. Methods: SGI-1027 was encapsulated into human serum albumin (HSA) nanoparticle (HSANP) functionalized with the PP1 peptide, a macro

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Lakshmikuttyamma, Asha, Stuart Scott, David P. Sheridan, John DeCoteau, and Ron Geyer. "Strategies to Re-Express Epigenetically-Silenced Tumor Suppressor Genes Converge on the Requirement for Inhibition of the Histone Methyltransferase SUV39H1." Blood 112, no. 11 (2008): 3357. http://dx.doi.org/10.1182/blood.v112.11.3357.3357.

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Abstract Gene silencing mediated by aberrant promoter DNA hypermethylation represents a key mechanism by which tumor suppressor gene expression is silenced in cancer and it is associated with multiple repressive histone modifications. Histone H3 lysine 9 (H3K9) methylation is a key repressive chromatin modification with important implications for regulating cell proliferation, differentiation, and gene expression. SUV39H1 is a methyltransferase that catalyzes the addition of trimethyl groups to H3K9. SUV39H1 is associated with regions of hypermethylated CpG islands, with repressive complexes,

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Zuzina, Alena B., Aliya Kh Vinarskaya, and Pavel M. Balaban. "DNA Methylation Inhibition Reversibly Impairs the Long-Term Context Memory Maintenance in Helix." International Journal of Molecular Sciences 24, no. 18 (2023): 14068. http://dx.doi.org/10.3390/ijms241814068.

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This work aims to study the epigenetic mechanisms of regulating long-term context memory in the gastropod mollusk: Helix. We have shown that RG108, an inhibitor of DNA methyltransferase (DNMT), impaired long-term context memory in snails, and this impairment can be reversed within a limited time window: no more than 48 h. Research on the mechanisms through which the long-term context memory impaired by DNMT inhibition could be reinstated demonstrated that this effect depends on several biochemical mechanisms: nitric oxide synthesis, protein synthesis, and activity of the serotonergic system. M

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Paul, Thomas A., Horatiu Muresan, Emily Prentice, and Linda Wolff. "Histone Modifications Associated with DNA Methylation and Transcriptional Repression of p15INK4b in Acute Myeloid Leukemia." Blood 112, no. 11 (2008): 3354. http://dx.doi.org/10.1182/blood.v112.11.3354.3354.

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Abstract p15INK4b is a cyclin-dependent kinase inhibitor known to regulate the G1-to-S transition of the cell cycle and to be involved in negatively regulating myeloid progenitor cell production. DNA hypermethylation leading to transcriptional silencing of p15INK4b has been reported in up to 70% of acute myeloid leukemia (AML) patient samples. In our study we sought to determine if p15INK4b DNA methylation in AML is accompanied by repressive histone modifications that contribute to the transcriptional repression of the gene at the chromatin level. Chromatin immunoprecipitation and DNA tiling m

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Mazewski, Candice, Frank Eckerdt, Aneta Baran, et al. "Abstract 3281: DNMT targeting enhances vulnerability of glioblastoma cells to MNK inhibition." Cancer Research 82, no. 12_Supplement (2022): 3281. http://dx.doi.org/10.1158/1538-7445.am2022-3281.

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Abstract Many factors complicate therapeutic strategies for glioblastoma (GBM), including the existence of the blood brain barrier and a heterogenous population of difficult to treat glioma stem cells. Innovative strategies targeting novel pathways alone or in combination are needed for sustainable therapeutic improvements. The MAPK pathway has been implicated in many cancers. MAPK interacting kinases (MNK1 and MNK2) are downstream of MAPKs and phosphorylate the eukaryotic translation initiation factor 4E (eIF4E), a protein involved in translation of oncogenic mRNAs. We have previously establi

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Martin, Lee J., Danya A. Adams, Mark V. Niedzwiecki, and Margaret Wong. "Aberrant DNA and RNA Methylation Occur in Spinal Cord and Skeletal Muscle of Human SOD1 Mouse Models of ALS and in Human ALS: Targeting DNA Methylation Is Therapeutic." Cells 11, no. 21 (2022): 3448. http://dx.doi.org/10.3390/cells11213448.

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Amyotrophic lateral sclerosis (ALS) is a fatal disease. Skeletal muscles and motor neurons (MNs) degenerate. ALS is a complex disease involving many genes in multiple tissues, the environment, cellular metabolism, and lifestyles. We hypothesized that epigenetic anomalies in DNA and RNA occur in ALS and examined this idea in: (1) mouse models of ALS, (2) human ALS, and (3) mouse ALS with therapeutic targeting of DNA methylation. Human superoxide dismutase-1 (hSOD1) transgenic (tg) mice were used. They expressed nonconditionally wildtype (WT) and the G93A and G37R mutant variants or skeletal mus

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Dermani, Fateme Karimi, Sibapriya Chaudhuri, Luika Timmerman, Scott Thomas, and Pamela Munster. "Abstract 5153: Synergistic efficacy of PARP and DNMT inhibition in ATM and CHEK2 CRISP-engineered in vitro and in vivo models." Cancer Research 85, no. 8_Supplement_1 (2025): 5153. https://doi.org/10.1158/1538-7445.am2025-5153.

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Introduction: More than a decade of work has demonstrated the benefit of using poly (ADP-ribose) polymerase inhibitors (PARPi) in patients with BRCA1 and BRCA2 mutant tumors, based on their compromised ability to repair DNA damage by homologous recombination (HRD). While the benefits of PARPi monotherapy can be limited, our laboratory is working to identify co-therapeutics to improve therapeutic efficacy. Homologous recombination requires the function of many other proteins besides BRCA1 and BRCA2, and PARP sensitivity of tumors with these mutations has not been well explored. Of particular in

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Banzon, Virryan, Vinzon Ibanez, Kestis Vaitkus, Kenneth Peterson, Joseph DeSimone та Donald Lavelle. "siRNA Targeting DNA Methyltransferase I Increases ε- and γ-Globin Expression." Blood 114, № 22 (2009): 973. http://dx.doi.org/10.1182/blood.v114.22.973.973.

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Abstract Abstract 973 Pharmacological inhibitors of DNA methyltransferase (DNMT) increase fetal hemoglobin (HbF) levels in experimental primates and patients with sickle cell disease. Therefore we hypothesize that DNMT is directly involved in maintaining repression of the γ-globin gene in adult stage erythroid cells. To test this hypothesis, levels of DNMT1 in mouse chemical-of-dimerization (CID) bone marrow (BM) cells containing the human β-globin gene locus in the context of a yeast artificial chromosome (βYAC) and primary cultured erythroid progenitor cells (EPC) derived from baboon CD34+ B

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Roy, Arya Mariam, Dharmesh Gopalakrishnan, Karan Jatwani, et al. "A phase Ib trial of enzalutamide with oral decitabine/cedazuridine in metastatic castration-resistant prostate cancer (CRPC)." Journal of Clinical Oncology 42, no. 4_suppl (2024): TPS252. http://dx.doi.org/10.1200/jco.2024.42.4_suppl.tps252.

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TPS252 Background: Exposure to androgen receptor (AR)-pathway inhibitors like enzalutamide (Enza) is associated with the emergence of ARlow subclones that coexist with ARhigh subclones in CRPC. These ARlow cells, including those in neuroendocrine prostate cancer (NEPC), are not critically dependent on AR signaling for survival and proliferation. Alterations in RB1, TP53, and PTEN tend to co-occur in human ARlow CRPC and NEPC. These as well as tumors from triple knockout mouse models demonstrate altered expression of epigenetic reprogramming factors, including consistent upregulation of DNA met

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Saavedra, Oscar M., Ljubomir Isakovic, David B. Llewellyn, et al. "SAR around (l)-S-adenosyl-l-homocysteine, an inhibitor of human DNA methyltransferase (DNMT) enzymes." Bioorganic & Medicinal Chemistry Letters 19, no. 10 (2009): 2747–51. http://dx.doi.org/10.1016/j.bmcl.2009.03.113.

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