ArticleJournal of experimental & clinical cancer research : CR2025
CCNY-mediated phosphorylation and TET2-BACH1-driven DNA demethylation activate PRC1 to augment NSCLC progression.
Article in Journal of experimental & clinical cancer research : CR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- PRC1 promotes immunosuppressive macrophages in sepsis via β-catenin/STAT3 signaling.Cellular and molecular life sciences : CMLS · 2026Article
- TET2: a critical regulatory hub with broad therapeutic implications across human diseases.Frontiers in immunology · 2026Review
- Integrated machine learning and single-cell analysis identify chromatin-remodeling gene signature for diagnosis and prognosis in nasopharyngeal carcinoma.Clinical and experimental medicine · 2025Article
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9 authors.
Funding
Abstract
backgroundThe 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.
methodsPRC1 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 were generated for in vivo verification. Tissue microarray (TMA) and bioinformatics analyses were employed to evaluate the clinical prognostic value of CCNY, TET2, and PRC1 in NSCLC.
resultsPRC1 was highly expressed in NSCLC cells. Silencing either PRC1 or CCNY, which promotes PRC1 phosphorylation, substantially reduced cell growth in vitro, impaired spindle formation, promoted G2/M phase cell cycle arrest, increased multi-nucleated cells, and weakened tumorigenic activity of cells. Moreover, TET2 was found to induce DNA demethylation of PRC1 and activate its transcription by interacting with BACH1. Inhibition of TET2, BACH1, or the PLK1-PRC1 interaction weakened the tumorigenic potential of NSCLC cells in vivo. The TMA analysis revealed increased levels of CCNY, TET2, and phosphorylated PRC1 in tumor tissues. Bioinformatics analyses suggested that these molecules were correlated with unfavorable prognosis in NSCLC patients.
conclusionThis study demonstrates a critical oncogenic role of PRC1 in NSCLC. CCNY, which modulates PRC1 phosphorylation, and the TET2-BACH1 cascade, which modulates demethylation and transcription of PRC1, may serve as promising targets for NSCLC management.
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