Abstract
Epithelial mesenchymal transition (EMT), the adoption by epithelial cells of a mesenchymal-like phenotype, is a process co-opted by carcinoma cells in order to initiate invasion and metastasis. In addition, it is becoming clear that is instrumental to both the development of drug resistance by tumour cells and in the generation and maintenance of cancer stem cells. EMT is thus a pivotal process during tumour progression and poses a major barrier to the successful treatment of cancer. Non-coding RNAs (ncRNA) often utilize epigenetic programs to regulate both gene expression and chromatin structure. One type of ncRNA, called long non-coding RNAs (lncRNAs), has become increasingly recognized as being both highly dysregulated in cancer and to play a variety of different roles in tumourigenesis. Indeed, over the last few years, lncRNAs have rapidly emerged as key regulators of EMT in cancer. In this review, we discuss the lncRNAs that have been associated with the EMT process in cancer and the variety of molecular mechanisms and signalling pathways through which they regulate EMT, and finally discuss how these EMT-regulating lncRNAs impact on both anti-cancer drug resistance and the cancer stem cell phenotype.
Highlights
Epithelial-Mesenchymal Transition: Cancer’s Gateway to MetastasisEpithelial-mesenchymal transition (EMT) is a process whereby epithelial cells shed many of their epithelial traits and acquire various features of mesenchymal cells
A greater understanding of the molecular mechanisms governing Epithelial mesenchymal transition (EMT) remains an imperative for the development of novel therapies, which can slow or prevent metastasis, the current great unmet need of cancer therapy
LncRNAs have emerged as integral players in the complex signalling network governing the activation of EMT in tumourigenesis and metastasis (Figure 1, Table 1)
Summary
Epithelial-mesenchymal transition (EMT) is a process whereby epithelial cells shed many of their epithelial traits and acquire various features of mesenchymal cells. During EMT, epithelial cells lose their polarity and many of their intercellular contacts such as desmosomes, adherens junctions and tight junctions, resulting in their disassociation from epithelial sheets They subsequently assume a number of mesenchymal properties, including enhanced migratory capacity, invasiveness, heightened resistance to apoptosis and greatly increased production of extracellular matrix components [1,2,3,4]. Carcinoma cells expressing markers of mesenchymal cells, such as vimentin, α-SMA, FSP1 and desmin, are frequently seen at the invasive fronts of tumours These are believed to be tumour cells in the process of undergoing EMT and it is thought that these cells will subsequently enter into the invasion-metastasis cascade and give rise to metastatic disease [2,10]
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