Epigenetic Regulation of EMT in Non-Small Cell Lung Cancer

被引:50
作者
O'Leary, Karen [1 ]
Shia, Alice [2 ]
Schmid, Peter [2 ]
机构
[1] NUI Galway, Div Pathol, Lambe Inst Translat Res, Galway, Ireland
[2] Queen Mary Univ London, Barts Canc Inst, Mol Oncol Expt Canc Med Ctr, London, England
关键词
NSCLC; EMT regulation; epigenetics; targeted therapy; lung cancer; tumor; EPITHELIAL-MESENCHYMAL TRANSITION; NF-KAPPA-B; TGF-BETA; E-CADHERIN; DNA METHYLATION; MIR-200; FAMILY; ACQUIRED-RESISTANCE; EGFR INHIBITION; GENE-EXPRESSION; REPRESSORS ZEB1;
D O I
10.2174/1568009617666170203162556
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Lung cancer remains the most diagnosed cancer in the world, with a high mortality rate and fewer therapeutic options. The most common lung cancer is non-small cell, consisting of adenocarcinoma, squamous cell carcinoma and large cell lung carcinoma. As per all solid tumours, the changes that occur for the initiation and metastasis of lung cancer can be described using the EMT (epithelial mesenchymal transition). Cells progressing through EMT lose their epithelial cell characteristics, expressing more mesenchymal markers and are phenotypically different. The transition can be controlled by changes in various pathways, such as TGF-beta, PI3K, MAPK, Hedgehog and Wnt. The changes in those pathways can be controlled epigenetically, via DNA methylation, histone modifications or changes in small/ non-coding RNA. We will describe the epigenetic changes that occur in these pathways and how we can consider novel methods to generate a synthetic lethality target in an epigenetically regulated pathway in EMT.
引用
收藏
页码:89 / 96
页数:8
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