Roche Joëlle, Gemmill Robert M, Drabkin Harry A
Laboratoire Ecologie et Biologie des Interactions, Equipe SEVE, Université de Poitiers, UMR CNRS 7267, F-86073 Poitiers, France.
Division of Hematology-Oncology, Medical University of South Carolina, 39 Sabin St., MSC 635, Charleston, SC 29425, USA.
Cancers (Basel). 2017 Jun 24;9(7):72. doi: 10.3390/cancers9070072.
Lung cancer is the leading cause of cancer deaths worldwide. It is an aggressive and devastating cancer because of metastasis triggered by enhanced migration and invasion, and resistance to cytotoxic chemotherapy. The epithelial to mesenchymal transition (EMT) is a fundamental developmental process that is reactivated in wound healing and a variety of diseases including cancer where it promotes migration/invasion and metastasis, resistance to treatment, and generation and maintenance of cancer stem cells. The induction of EMT is associated with reprogramming of the epigenome. This review focuses on major mechanisms of epigenetic regulation mainly in lung cancer with recent data on EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit ), the catalytic subunit of the PRC2 (Polycomb Group PcG), that behaves as an oncogene in lung cancer associated with gene repression, non-coding RNAs and the epitranscriptome.
肺癌是全球癌症死亡的主要原因。由于迁移和侵袭增强引发的转移以及对细胞毒性化疗的耐药性，它是一种侵袭性且具有毁灭性的癌症。上皮-间质转化（EMT）是一个基本的发育过程，在伤口愈合以及包括癌症在内的多种疾病中被重新激活，在癌症中它促进迁移/侵袭和转移、耐药性以及癌症干细胞的产生和维持。EMT的诱导与表观基因组的重编程有关。本综述主要关注肺癌中表观遗传调控的主要机制，并结合有关EZH2（zeste 2增强子多梳抑制复合体2亚基）的最新数据，EZH2是PRC2（多梳蛋白家族PcG）的催化亚基，在肺癌中作为一种癌基因，与基因抑制、非编码RNA和表观转录组有关。
