Abstract
Despite major advances, non-small cell lung cancer (NSCLC) remains the major cause of cancer-related death in developed countries. Metastasis and drug resistance are the main factors contributing to relapse and death. Epithelial-to-mesenchymal transition (EMT) is a complex molecular and cellular process involved in tissue remodelling that was extensively studied as an actor of tumour progression, metastasis and drug resistance in many cancer types and in lung cancers. Here we described with an emphasis on NSCLC how the changes in signalling pathways, transcription factors expression or microRNAs that occur in cancer promote EMT. Understanding the biology of EMT will help to define reversing process and treatment strategies. We will see that this complex mechanism is related to inflammation, cell mobility and stem cell features and that it is a dynamic process. The existence of intermediate phenotypes and tumour heterogeneity may be debated in the literature concerning EMT markers, EMT signatures and clinical consequences in NSCLC. However, given the role of EMT in metastasis and in drug resistance the development of EMT inhibitors is an interesting approach to counteract tumour progression and drug resistance. This review describes EMT involvement in cancer with an emphasis on NSCLC and microRNA regulation.
Highlights
Epithelial-to-mesenchymal transition (EMT) is an evolutionarily conserved but complex molecular and cellular program in which cells undergo conversion from epithelial to mesenchymal state [1].Epithelial differentiated characteristics are lost, including cell-cell adhesion, planar and apical-basal polarity and lack of mobility
Recent evidences show that transcription factors linked to EMT may directly be involved in carcinogenesis
Growth Factor Receptor (EGFR)-mutated lung adenocarcinoma, we previously reported on surgical samples that TWIST1 expression was linked to EGFR mutations, low E-cadherin expression and low disease-free survival [44]
Summary
Epithelial-to-mesenchymal transition (EMT) is an evolutionarily conserved but complex molecular and cellular program in which cells undergo conversion from epithelial to mesenchymal state [1]. EMT was initially described as a cell culture phenomenon before being recognized in vivo and studied in embryonic development This process is obviously reversible and is highly conserved from diploblasts (medusa) 800 million years ago to nowadays [2]. It aims at dissociating epithelium and degrading basement membranes so that cells acquire a fibroblastic or glial-cell phenotype and migrate. This state was defined as “mesenchyme” (from Greek, μεσo, μεσo, middle and ενκηυμα in fusion) to describe a poorly organized state between two tissues. Both play an important play in organogenesis (i.e., in renal epithelium or cardiac organogenesis formation) [4] and in cancer [5,6]
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