Abstract
Metastasis is a multistep process starting with the dissemination of tumor cells from a primary site and ending with secondary tumor development in an anatomically distant location. The epithelial–mesenchymal transition (EMT), a process that endows epithelial tumor cells with mesenchymal properties including reduced adhesion and increased motility, is considered a critical step driving the early phase of cancer metastasis. Although significant progress has been made in understanding the molecular characteristics of EMT, the intracellular mechanisms driving transition through the various stages of EMT remain unclear. In recent years, an increasing number of studies have demonstrated the involvement of long non-coding RNAs (lncRNAs) in tumor metastasis through modulating EMT. LncRNAs and their associated signaling networks have now emerged as new players in the induction and regulation of EMT during metastasis. Here we summarize the recent findings and characterizations of several known lncRNAs involved in the regulation of EMT. We will also discuss the potential use of these lncRNAs as diagnostic and prognostic biomarkers as well as therapeutic targets to slow down or prevent metastatic spread of malignant tumors.
Highlights
epithelial–mesenchymal transition (EMT) facilitates cancerous epithelial cells to enter into a mesenchymal-like state by endowing them migratory and invasive properties, which enables primary tumor cells to move and colonize distant organs and form secondary tumor metastases
The activated Hh increases Gli expression, and enhances the expression of SOX2 and OCT4 to maintain cancer stem cells (CSCs). These results indicate that long non-coding RNAs (lncRNAs)-Hh impinges upon EMT and CSC stemness by modulating the hedgehog signaling
EMT is a complex, multifunctional, and tightly regulated process that plays a critical role in metastatic spread of cancer cells
Summary
There are growing interests in lncRNAs as potential biomarkers and therapeutic targets of EMT and cancer metastasis, it remains largely unknown how they are regulated in cancer cells and how they affect EMT and metastasis. We will provide a comprehensive review of the known lncRNAs relevant to EMT in cancer metastasis and discuss the molecular mechanisms underlying their regulation of EMT and their therapeutic implications as biomarkers and potential drug targets. It remains to be determined the different and precise molecular mechanisms by which functional lncRNAs switch EMT on and off during tumor development. Deeper understanding the molecular mechanisms that control EMT will shed lights to the metastatic processes of tumor cells, and provide new therapeutic targets and treatment options for effective cancer therapy.
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