CCNY-mediated phosphorylation and TET2-BACH1-driven DNA demethylation activate PRC1 to augment NSCLC progression.

ABSTRACT:

Background

The protein regulator of cytokinesis 1 (PRC1) is a prognostic marker characterized by low DNA methylation in lung cancer. This study aims to examine the function of PRC1 in non-small cell lung cancer (NSCLC) cells and investigates its regulatory mechanisms.

Methods

PRC1 expression in NSCLC cells was assessed using qPCR and western blot analyses. Loss- and gain-of-function assays of PRC1 were performed in NSCLC cells to analyze its effect on cell cycle progression and growth. Genetic knockdown or pharmaceutical inhibition of cyclin Y (CCNY), tet methylcytosine dioxygenase 2 (TET2), and BTB domain and CNC homolog 1 (BACH1) was conducted to analyze their influence on PRC1 phosphorylation or transcription. Subcutaneous xenograft and orthotopic isograft tumor models we

SUBMITTER: Huang D 

PROVIDER: S-EPMC12261648 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature