Abstract
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-β, 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.
Keywords: NSCLC, EMT regulation, epigenetics, targeted therapy, lung cancer, tumor.
Graphical Abstract
Current Cancer Drug Targets
Title:Epigenetic Regulation of EMT in Non-Small Cell Lung Cancer
Volume: 18 Issue: 1
Author(s): Karen O’Leary, Alice Shia and Peter Schmid*
Affiliation:
- Molecular Oncology/ Experimental Cancer Medicine Centre, Barts Cancer Institute, Queen Mary University of London, London,United Kingdom
Keywords: NSCLC, EMT regulation, epigenetics, targeted therapy, lung cancer, tumor.
Abstract: 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-β, 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.
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Cite this article as:
O’Leary Karen , Shia Alice and Schmid Peter *, Epigenetic Regulation of EMT in Non-Small Cell Lung Cancer, Current Cancer Drug Targets 2018; 18 (1) . https://dx.doi.org/10.2174/1568009617666170203162556
DOI https://dx.doi.org/10.2174/1568009617666170203162556 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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