Faculty, Staff and Student Publications

Publication Date

6-1-2025

Journal

NAR Cancer

DOI

10.1093/narcan/zcaf018

PMID

40433167

PMCID

PMC12107434

PubMedCentral® Posted Date

5-27-2025

PubMedCentral® Full Text Version

Post-print

Abstract

DNA methylation alterations, including hypermethylation and silencing of tumor suppressor genes, contribute to cancer formation and progression. The FDA-approved nucleoside analogs azacytidine and decitabine are effective demethylating agents for hematologic malignancies but their general use has been limited by their toxicity and ineffectiveness against solid tumors. GSK-3484862, a dicyanopyridine-containing, DNMT1-selective inhibitor and degrader, offers a promising lead for developing novel demethylating therapeutics. Here, we demonstrate that GSK-3484862 treatment upregulates DNMT3B expression in lung cancer cell lines (A549 and NCI-H1299). Disrupting DNMT3B in NCI-H1299 sensitizes these cells to GSK-3484862, enhancing its inhibitory effects on cell viability and growth. GSK-3484862 treatment induces demethylation at DNMT3B regulatory elements including a candidate enhancer located ∼10 kb upstream of the DNMT3B transcription start site, as well as at the promoter of TERT (telomerase reverse transcriptase), a potential activator of DNMT3B expression. These demethylation events correlate with upregulation of DNMT3B expression. These findings suggest that combining inhibitors targeting DNMT1, the maintenance methyltransferase, with those targeting DNMT3A/3B, the de novo methyltransferases, or using pan-DNMT inhibitors, could enhance anticancer efficacy and reduce resistance.

Keywords

Humans, DNA (Cytosine-5-)-Methyltransferases, Lung Neoplasms, DNA Methyltransferase 3B, DNA (Cytosine-5-)-Methyltransferase 1, Gene Expression Regulation, Neoplastic, Cell Line, Tumor, DNA Methylation, Pyridines, Cell Proliferation, Cell Survival, A549 Cells, Promoter Regions, Genetic, Up-Regulation

Published Open-Access

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