Epigenetic Regulation of EMT in Non-Small Cell Lung Cancer

Author:

O’Leary Karen1,Shia Alice2,Schmid Peter3

Affiliation:

1. Lambe Institute for Translational Research, Division of Pathology, NUI Galway, Ireland

2. Molecular Oncology/Experimental Cancer Medicine Centre, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom

3. Molecular Oncology/ Experimental Cancer Medicine Centre, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom

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.

Publisher

Bentham Science Publishers Ltd.

Subject

Cancer Research,Drug Discovery,Pharmacology,Oncology

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