DNMT1 (DNA methyltransferase 1)

Collectively, the findings demonstrate that LKB1 deficiency promotes ferroptosis resistance in lung cancer cells. Radiotherapy simultaneously disrupts ferroptosis tolerance through the DNMT1-OSGIN1 axis and activates the STING pathway, effectively reversing ICI resistance in LKB1-deficient lung tumors.

Correlation and regression analyses validated the proposed ceRNA interactions and their significant association with advanced cancer stage. A high-risk score from the H19/miR-152/DNMT1 axis was prognostic only in thyroid cancer (HR = 2.97).

Conversely, in prostate adenocarcinoma models, DNMT1 deletion leads to de-repression of neuroendocrine lineage genes with a loss of H3K27me3 marks. Our findings reveal a functional interplay between two repressive epigenetic machineries that mediates lineage plasticity in prostate cancer.

Notably, recombinant TRAIL protein synergizes with SGI1027 or MS1129 to kill VHL-deficient ccRCC in mice. Collectively, our study unveils an apoptosis induction strategy that involves hijacking HIFs for ccRCC treatment.

Waterpipe smoke may result in a DNA hypomethylation pattern in initial exposure periods, contributing to activate proto-oncogenes and/or genomic instability. Over long periods, it may lead to a methylation pattern similar to that of control or even to hypermethylation, silencing tumor suppressor genes. These alterations in the genome due to hypo/hypermethylation contribute largely for the development of diseases such as oral cancer.

Compared to normal tissue an increased expression of NOX4, OGG1, MSH2/MSH6 proteins and phospho-Smad3 was found in RAI Refractory BRAFV600E mutated tumors. Collectively, our findings reveal a mechanistic basis for NOX4's role in thyroid dedifferentiation.

We also demonstrated that DAXX loss increased decitabine sensitivity in the myeloid leukemia (AML) cell line THP-1. Together, these findings show that DAXX promotes SUMOylation of DNMT1 trapped on DNA under both covalent and non-covalent trapping conditions.

The seven hub RBP genes are potential biomarkers for CRC, providing new insights and therapeutic targets. However, functional validation and larger sample sizes are needed for clinical application.

ECRG4 inhibits breast cancer progression by positively regulating NFIC/PTEN to suppress the SHP2/PI3K/SP1 signaling pathway. Targeting this signaling axis may provide a new strategy for breast cancer treatment.

Importantly, glycolysis inhibition restores senescence and reverses PDP1-driven malignant phenotypes. Collectively, these findings identify that PDP1 drives senescence-associated malignant progression in HCC by linking glycolytic regulation, histone lactylation, and DNA methylation to the control of ADCY5 expression and subsequent cAMP/Ca2+ signaling, underscoring its potential as a therapeutic target.

Ectopic expressions of DNMT1 impose an epigenetic checkpoint at those target loci by methylation of promoter DNA of the respective genes. We conclude that, gene specific hypomethylation of some genes, including COL1A1, COL1A2, COL4A1, SPP1, SPARC, and THBS2 drives COAD and would serve as potential markers for COAD screening.