Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article 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 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.
Results: PRC1 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.
Conclusion: This 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.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12261648 | PMC |
| http://dx.doi.org/10.1186/s13046-025-03472-x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Ultrasound-Enhanced Delivery of Salvianolic Acid F Targets CXCL5 to Suppress Lung Cancer Progression: Insights from PC9 and H1299 Models.
Cancer Biother Radiopharm
September 2025
School of Food Science, Nanjing Xiaozhuang University, Nanjing, China.
Lung cancer remains one of the leading causes of cancer-related mortality worldwide, highlighting the urgent need for more effective and targeted therapeutic strategies. Traditional Chinese Medicine (TCM), known for its favorable safety profile and broad pharmacological effects, offers promising candidates for cancer treatment. Salvianolic acid F (SAF), a key bioactive compound derived from , has demonstrated antitumor potential, but its role and underlying mechanisms in lung cancer remain inadequately characterized.
View Article and Find Full Text PDFPembrolizumab treatment in SMARCA4-deficient nonsmall cell lung cancer: high tumor mutational burden and programmed death-ligand 1(+) expression on circulating tumor cells for real-time monitoring: a case report.
Anticancer Drugs
September 2025
Department of Thoracic Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College.
Nonsmall cell lung cancer (NSCLC) with SMARCA4 deficiency represents a rare subset of lung tumors characterized by early metastasis, poor response to chemotherapy, and unfavorable prognosis. Established therapy strategies for SMARCA4-deficient NSCLC remain elusive. While immune checkpoint inhibitors have been proposed as a potential solution, their efficacy remains uncertain.
View Article and Find Full Text PDFAucubin inhibits the activity of lung cancer stem-like cells by targeting degradation of β-catenin.
J Pharm Pharmacol
September 2025
Department of Clinical Pharmacy, Hebei Medical University Third Hospital. No. 139 Ziqiang Road, Qiaoxi District, Shijiazhuang 050051, China.
Objectives: To investigate the antitumor effects of aucubin (AC) in non-small cell lung cancer (NSCLC) and uncover its plausible mechanism against lung cancer stem-like cells (LCSCs).
Methods: In vitro experiments included MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, a reagent commonly used for cell viability assay) and colony formation assays to assess anti-proliferative effects on A549 and NCI-H1975 lung cancer cell lines, wound healing and Transwell invasion assays to evaluate inhibition of cell migration and invasion, tumorsphere-formation experiments to detect changes in NSCLC cell stemness, as well as Western blot and quantitative reverse transcription polymerase chain reaction (qRT-PCR) analyses to measure the expression of LCSC markers (CD44, CD133, Oct4, and Nanog). In vivo experiments were conducted to observe the impact of AC on NSCLC metastasis and mouse survival rates.
Integrative profiling of lung cancer biomarkers EGFR, ALK, KRAS, and PD-1 with emphasis on nanomaterials-assisted immunomodulation and targeted therapy.
Front Immunol
September 2025
Department of Thoracic Surgery, Shenzhen People's Hospital (The First Affiliated Hospital, Southern University of Science and Technology; The Second Clinical Medical College, Jinan University), Shenzhen, Guangdong, China.
Background: Lung cancer remains the leading cause of cancer-related mortality globally, primarily due to late-stage diagnosis, molecular heterogeneity, and therapy resistance. Key biomarkers such as EGFR, ALK, KRAS, and PD-1 have revolutionized precision oncology; however, comprehensive structural and clinical validation of these targets is crucial to enhance therapeutic efficacy.
Methods: Protein sequences for EGFR, ALK, KRAS, and PD-1 were retrieved from UniProt and modeled using SWISS-MODEL to generate high-confidence 3D structures.
Nuclear glycine decarboxylase suppresses STAT1-dependent MHC-I and promotes cancer immune evasion.
EMBO J
September 2025
Department of Infectious Diseases, Medical Research Institute, Zhongnan Hospital of Wuhan University; Frontier Science Center for Immunology and Metabolism, Taikang Center for Life and Medical Sciences; Wuhan University, Wuhan, 430071, China.
Inadequate antigen presentation by MHC-I in tumor microenvironment (TME) is a common immune escape mechanism. Here, we show that glycine decarboxylase (GLDC), a key enzyme in glycine metabolism, functions as an inhibitor of MHC-I expression in EGFR-activated tumor cells to induce immune escape by a mechanism independent of its enzymatic activity. Upon EGFR activation, GLDC is phosphorylated by SRC and subsequently translocated to the nucleus in human NSCLC cells.
View Article and Find Full Text PDF