DNMT1
DNA methyltransferase 1 (DNMT1) is a DNA methyltransferase and a central target in studies of DNA methylation–associated disease mechanisms.
DNA methyltransferase 1 (DNMT1) is a DNA methyltransferase and a central target in studies of DNA methylation–associated disease mechanisms. The recent literature supplied here places DNMT1 within a single broad theme of epigenetic disease mechanisms, in which altered DNMT1 expression or activity is associated with cancer biology, metabolic dysfunction, fibrosis, vascular disease, and neurodegeneration. These studies examine DNMT1 alongside DNA methylation, global DNA methylation, DNMT3A, ubiquitin-specific peptidase 7 (USP7), and signaling or metabolic pathways involving TP53, Hippo signaling, the urea cycle, propionate metabolism, and glycolytic reprogramming.
DNMT1 is being investigated both as a mechanistic regulator and as a pharmaceutical target. Hypomethylating strategies, including DNMT1 inhibitors and the investigational agent NTX-301, are being evaluated in relation to apoptosis and cancer-cell responses, while other studies examine indirect modulation of DNMT1 through USP7, stress signaling, or candidate drugs such as sotagliflozin and pirfenidone. The reported findings are disease-specific and include associations with chemotherapy response, tumor recurrence, fibrosis, diabetic complications, fatty-liver disease, and Parkinsonism; they do not establish a single therapeutic mechanism applicable across these conditions.
Rebuilt from PubMed 18 Sept 2026 · no new papers today
Where the papers sit
9 papers study dnmt1 directly. Those 9 are one subject: DNA Methylation in Disease. DNA methylation links DNMT1 to cancer growth, treatment response, recurrence, fibrosis and metabolic dysfunction. The recurring focus is on DNMT1 complexes and inhibitors as ways to alter gene expression, metabolism and therapeutic sensitivity. No way of splitting those 9 scores better than chance.
Recent Findings on DNMT1
In acute myeloid leukemia (AML), the investigational hypomethylating agent NTX-301 was reported to inhibit DNMT1 and increase p73 and caspase 8 (CASP8), including activated CASP8, in both TP53-wild-type and TP53-mutant AML models. The study also reported activation of p53 signaling and described preclinical activity in venetoclax-resistant and TP53-mutant AML, linking DNMT1 inhibition to apoptotic signaling involving TP53, p73, CASP8, and the BCL2 apoptosis regulator pathway 42439804Jul.
A study of Jianpi Qinghua granule (JPQH) in metabolic dysfunction-associated fatty liver disease examined a DNMT–urea cycle axis. JPQH reduced DNMT1 and DNMT3A expression, attenuated promoter hypermethylation of genes encoding urea-cycle enzymes, and restored their transcriptional and protein expression. These findings connected modulation of DNA methylation with hepatic nitrogen metabolism and the urea cycle 42107753May.
In hepatocellular carcinoma (HCC), research on recurrence after microwave ablation identified an HSP90α–USP7–DNMT1 axis. The study reported that HSP90α collaborated with USP7 to stabilize and increase DNMT1, converting sublethal heat-stress signaling after interventional microwave ablation into an epigenetic response characterized by increased DNA methylation. This pathway was further linked to disruption of ACSS3-mediated propionate metabolism 42363602Jun.
In lung adenocarcinoma, DNMT1 was investigated in relation to QDPR downregulation and chemotherapy response. The researchers analyzed associations between DNA methylation-related enzymes and QDPR expression in the GSE33532, GSE43458, and GSE75037 datasets, followed by cross-dataset validation to identify potential upstream regulators. The reported work therefore positioned DNMT1 among candidate regulatory factors associated with QDPR expression and treatment response 42678580Sep.
A study of sotagliflozin, a dual SGLT1/2 inhibitor, examined DNMT1 together with DNMT3A and DNMT3B and with class I/II histone deacetylases in breast- and lung-cancer cells. The study associated modulation of these epigenetic enzymes with anticancer effects. Molecular-docking analysis predicted favorable interactions between sotagliflozin and the DNA methyltransferases, with the strongest predicted interaction involving DNMT1 and a calculated binding energy of −8.9 kcal/mol. This result was a computational prediction rather than a direct demonstration of biochemical binding 42677956Sep.
In endothelial cells associated with diabetic retinopathy, DNMT1 was investigated as an upstream regulator of the E3 ligase FBXO32. The study reported that DNMT1 methylated FBXO32 and linked this regulatory relationship to Myc stability and glycolytic reprogramming. The findings connect DNMT1-associated epigenetic regulation with high-glucose-related endothelial dysfunction and cellular energy metabolism 42348038Jun.
In diabetic kidney disease, pirfenidone was studied in relation to GLIS1, USP7, and DNMT1. The reported mechanism involved disruption of the USP7–DNMT1 complex, elevation of GLIS1, reduction of reactive oxygen species, and inhibition of TGF-β1/Smad signaling, with corresponding effects on renal fibrosis. Immunofluorescence staining was used to assess the expression and colocalization of USP7 and DNMT1 42159303May.
In a rat model of Parkinsonism generated by intranigral rotenone, urolithin A was evaluated for effects on a DNMT1–α-synuclein axis. The study specifically examined post-translational changes in DNMT1 as an epigenetic marker and reported that urolithin A reversed the rotenone-associated Parkinsonian phenotype in association with modulation of this axis 41880654Mar.
In papillary thyroid cancer, a DNMT1 inhibitor was used to investigate the consequences of sustained DNA hypomethylation. The study reported that prolonged hypomethylation induced apoptosis in thyroid-cancer cells and that DNMT1 overexpression in papillary thyroid cancer suggested involvement in thyroid carcinogenesis. The work supports investigation of DNMT1 inhibition as a strategy for altering tumor-cell viability, while the reported conclusions remain specific to the experimental thyroid-cancer context 42048599Apr.
Written from 9 PubMed abstracts, each one cited by PMID above. Published: 2026-09-16. Drafted by language models from published abstracts; not medical advice.