Epigenetic Regulation of the Epithelial to Mesenchymal Transition in Lung Cancer

Abstract

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.

Retracted Article: Long noncoding RNA ANRIL knockdown increases sensitivity of non-small cell lung cancer to cisplatin by regulating the miR-656-3p/SOX4 axis

“…Furthermore, EMT has been regarded as an important pathway associated with metastasis and drug resistance in cancers. [31][32][33] By detecting migration and protein levels of E-cadherin and MMP-9, this study showed that ANRIL silence suppressed CDDP resistance by decreasing EMT. Collectively, ANRIL knockdown could facilitate apoptosis and repress EMT to decrease CDDP resistance in NSCLC.…”

The Epithelial-to-Mesenchymal Transition in Cancer

“…The third series of reviews addresses more specific mechanisms involved in EMT regulation [ 14 , 15 , 16 , 17 ]. First, Roche et al present epigenetic regulation of EMT mainly in lung cancer with recent data on EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit) that behaves as an oncogene in lung cancer associated with gene repression [ 14 ]. EZH2 is the catalytic subunit of the PRC2 (polycomb group PcG), which methylates lysine 27 of histone H3, inducing a repressive transcriptional mark.…”

Small cell lung cancer tumors and preclinical models display heterogeneity of neuroendocrine phenotypes

“…Epithelial to mesenchymal transition (EMT) is a fundamental developmental process that is reactivated in wound healing and in a variety of diseases including cancer where it promotes migration/invasion and metastasis, lack of cell to cell adhesion, resistance to treatment, immune evasion and generation and maintenance of cancer stem cells (59,60). Many of these properties are present in the low NE subtype.…”