Chip-seq analysis of H3K4me3, H3K27me3, DNMT1 and EZH2 binding to chromatin following acute (10 days) and chronic (10 months) treatment of human bronchial epithelial cells (HBEC3KT) cells with 10 µg/ml cigarette smoke condensate (CSC).
收藏干细胞与再生医学数据中心2022-02-20 更新2024-03-06 收录
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资源简介：
We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells (HBEC) for transformation by a single oncogene. The smoke-induced, chromatin changes include initial repressive polycomb marking of genes later manifesting abnormal DNA methylation by 10 months. At this time, cells manifest epithelial to mesenchymal changes, anchorage-independent growth and upregulated RAS/MAPK signaling with silencing of hyper-methylated genes normally inhibiting these pathways and which are associated with smoking related NSCLC. These cells, in the absence of any driver gene mutations, now transform by introducing a single KRAS mutation and form adeno-squamous lung carcinomas in mice. Thus, epigenetic abnormalities may prime for changing oncogene senescence to addiction for a single key oncogene involved in lung cancer initiation.
提供机构：
Johns Hopkins Medicine
创建时间：
2022-02-20
