Abstract
Epithelial–mesenchymal transition (EMT) is a multistep process that allows epithelial cells to acquire mesenchymal properties. Fundamental in the early stages of embryonic development, this process is aberrantly activated in aggressive cancerous cells to gain motility and invasion capacity, thus promoting metastatic phenotypes. For this reason, EMT is a central topic in cancer research and its regulation by a plethora of mechanisms has been reported. Recently, genomic sequencing and functional genomic studies deepened our knowledge on the fundamental regulatory role of noncoding DNA. A large part of the genome is transcribed in an impressive number of noncoding RNAs. Among these, long noncoding RNAs (lncRNAs) have been reported to control several biological processes affecting gene expression at multiple levels from transcription to protein localization and stability. Up to now, more than 8000 lncRNAs were discovered as selectively expressed in cancer cells. Their elevated number and high expression specificity candidate these molecules as a valuable source of biomarkers and potential therapeutic targets. Rising evidence currently highlights a relevant function of lncRNAs on EMT regulation defining a new layer of involvement of these molecules in cancer biology. In this review we aim to summarize the findings on the role of lncRNAs on EMT regulation and to discuss their prospective potential value as biomarkers and therapeutic targets in cancer.
Highlights
Epithelial to Mesenchymal TransitionThe epithelial to mesenchymal transition (EMT) is a multistep, plastic and reversible process that allows epithelial cells to acquire mesenchymal characteristics
Epithelial–mesenchymal transition (EMT) is a multistep process that allows epithelial cells to acquire mesenchymal properties
EMT-TFs are a group of transcription factors among which SNAIL, SLUG, TWIST, zinc finger E-box-binding homeobox 1 and 2 (ZEB1, ZEB2) are well known to cooperate to a different extent in distinct cellular contexts to inhibit or induce the expression of a precise set of genes indispensable for EMT partial or complete execution
Summary
The epithelial to mesenchymal transition (EMT) is a multistep, plastic and reversible process that allows epithelial cells to acquire mesenchymal characteristics. Full EMT is rarely achieved and during this transition cells reside in a plethora of intermediate states that contribute to cancer heterogeneity [5]. This plasticity is granted by the capacity of cancer cells to modulate gene expression, transitioning from different states of partial EMT. In well differentiated carcinomas, cells at the invasion front often migrate in groups instead of as single cell, a phenomenon called collective cell migration [6,7,8] In this state, cells acquire altered apico-basal polarity, extracellular matrix and invasion and motility capacity, but remain connected to each other by epithelial Cadherins and cell-cell junctions [7,8]. Understanding all the aspects regulating this process could provide useful tools to counteract it in tumor cells, and to gain molecular information to distinguish aggressive cells prone to form metastasis
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