The inactivation of tumour suppressor genes by aberrant methylation of promoter regions has been described as a frequent event in neoplasia development, including lung cancer. The p16 gene is a tumour suppressor gene involved in the regulation of cell cycle progression that has been reported to be inactivated by promoter methylation in lung carcinomas at variable frequencies around the world in a smoking habit dependent manner. The purpose of this study was to investigate the methylation status of the promoter region of the p16 gene in 74 non-small cell lung carcinomas from Chile. The frequency of p16 gene inactivation by promoter methylation was determined as 79.7% (59/74). When we considered histological type, we observed that p16 promoter methylation was significantly higher in squamous cell carcinomas (30/33, 91%) compared with adenocarcinomas (21/30, 70%) (p=0.029). In addition, no association between p16 promoter methylation and gender, age or smoking habit was found (p=0.202, 0.202 and 0.147 respectively). Our results suggest that p16 promoter hypermethylation is a very frequent event in non-small cell lung carcinomas from Chile and could be smoking habit-independent.
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Front Oncol
December 2024
Penn State Hershey Cancer Institute, Pennsylvania State University College of Medicine, Hershey, PA, United States.
Unlabelled: Cladribine indirectly downregulates methylation of DNA, RNA, and histones by blocking the transfer of methyl groups from -adenosyl-methionine. The cladribine and rituximab combination showed a synergetic effect in treating B-cell lymphomas. Bortezomib (Velcade) is a Food and Drug Administration (FDA)-approved proteasome inhibitor for treating mantle cell lymphoma (MCL).
View Article and Find Full Text PDFBiochim Biophys Acta Mol Basis Dis
December 2024
State Key Laboratory of Respiratory Diseases Allergy Division at Shenzhen University and Institute of Allergy & Immunology of Shenzhen University School of Medicine, Shenzhen, China. Electronic address:
The pathogenesis of many immune disorders is linked to regulatory macrophage dysfunction. The mechanism underlying it is unclear. The objective of this study is to examine the mechanism by which the PRKN ubiquitin protein ligase (PRKN) inhibits the development of regulatory macrophages (Mreg).
View Article and Find Full Text PDFPlant Sci
December 2024
National Key Laboratory of Crop Genetics and Germplasm Enhancement, College of Horticulture, Nanjing Agricultural University, Nanjing, 210095, Jiangsu Province, China. Electronic address:
Forward genetic screens have uncovered numerous genes involved in DNA methylation regulation, but these methods are often time-intensive, costly, and labor-intensive. To address these limitations, this study utilized CRISPR technology to knockout selected co-expressed genes, enabling the rapid identification of low luciferase (LUC) luminescence mutants in the Col-LUC line, which harbors a LUC transgene driven by a 2×35S promoter in Arabidopsis. As proof of concept, the repressor of silencing 1 (ROS1) and RNA-directed DNA methylation 1 (RDM1) genes were used as controls, while the increased DNA methylation 3 (IDM3) gene, co-expressed with ROS1, was selected as the target for gene knockout experiments.
View Article and Find Full Text PDFTransl Oncol
December 2024
Department of Stomatology, Children's Hospital of Chongqing Medical University, Chongqing, PR China.
The low expression of period circadian regulator 3 (PER3) in head and neck squamous cell carcinoma is closely correlated with tumor size and invasion depth. Hypoxia-inducible factor 1 subunit alpha (HIF-1α) regulates epithelial-mesenchymal transition (EMT) transcription factors, activates EMT, and promotes tumor metastasis. Here, we investigated the role and molecular mechanism of PER3 in regulating HIF-1α and metastasis in oral squamous cell carcinoma (OSCC) by using bioinformatics analyses and in vitro and in vivo experiments.
View Article and Find Full Text PDFMol Cell
December 2024
Wellcome Centre for Cell Biology, School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3BF, UK; Epigenetics Programme, Babraham Institute, Cambridge CB22 3AT, UK. Electronic address:
Promoters of developmental genes in embryonic stem cells (ESCs) are marked by histone H3 lysine 4 trimethylation (H3K4me3) and H3K27me3 in an asymmetric nucleosomal conformation, with each sister histone H3 carrying only one of the two marks. These bivalent domains are thought to poise genes for timely activation upon differentiation. Here, we show that asymmetric bivalent nucleosomes recruit repressive H3K27me3 binders but fail to enrich activating H3K4me3 binders, thereby promoting a poised state.
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