The expression of DNMT1 was significantly higher in lung cancer tissues than in corresponding normal lung tissues.

suggest that targeting of the IL-6/JAK2/STAT3 signaling pathway and DNMT1 may become important strategies for treating lung cancer

These findings identify functional cross-talk between KIT and DNMT1 in the development of drug resistance, implying the reciprocal targeting of protein kinases and DNA methyltransferases as an essential strategy for durable responses in lung cancer.

Results show that DNMT1 is highly expressed in lung tumors compared to normal tissues, and that DBCCR1 attenuates its expression suggesting a reciprocal regulation between genetic silencing of cancer suppressor genes and activating DNA methylation.

the regulatory and functional interplay between DNA methylation and tyrosine kinase signaling in propelling tumorigenesis, providing a widely applicable approach for targeting lung cancer.

DNMT1 was downregulated in the lung cancer group and its expression was further reduced in the presence of increasing malignant burden as indicated by the endobronchial findings further suggesting an lung cancer-specific signature.

This work revealed the critical function of GOLM1/miR-200a/DNMT1 signaling pathway on regulating lung adenocarcinoma cell proliferation

HAGLR could physically interact with DNMT1, and recruit DNMT1 on E2F1 promoter to increase local DNA methylation. HAGLR promoted lung adenocarcinoma progression by recruiting DNMT1 to modulate the promoter methylation and expression of E2F1.

DNMT1 promotes cell proliferation via methylating hMLH1 and hMSH2 promoters in EGFR-mutated non-small cell lung cancer.