Noncoding RNAs in Tumor Epithelial-to-Mesenchymal Transition

• Published in: Stem cells international Vol. 2016; no. 2016; pp. 1 - 13
• Main Authors: Lin, Ching-Wen, Yang, Pan-Chyr, Lin, Pei-Ying
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01.01.2016; John Wiley & Sons, Inc; Wiley
• Subjects: Binding sites; Cancer; Cytokines; Development and progression; DNA binding proteins; Feedback; Fibroblasts; Gene expression; Genes; Genetic aspects; Genetic transcription; Genetic translation; Health aspects; Hospitals; Hypoxia; Insulin-like growth factors; Kidney cancer; Kinases; Metastasis; MicroRNA; Mortality; Phosphatase; Proteins; Review; Stem cells; Transcription factors
• ISSN: 1687-966X; 1687-9678; 1687-9678
• DOI: 10.1155/2016/2732705

Epithelial-derived tumor cells acquire the capacity for epithelial-to-mesenchymal transition (EMT), which enables them to invade adjacent tissues and/or metastasize to distant organs. Cancer metastasis is the main cause of cancer-related death. Molecular mechanisms involved in the switch from an epithelial phenotype to mesenchymal status are complicated and are controlled by a variety of signaling pathways. Recently, a set of noncoding RNAs (ncRNAs), including miRNAs and long noncoding RNAs (lncRNAs), were found to modulate gene expressions at either transcriptional or posttranscriptional levels. These ncRNAs are involved in EMT through their interplay with EMT-related transcription factors (EMT-TFs) and EMT-associated signaling. Reciprocal regulatory interactions between lncRNAs and miRNAs further increase the complexity of the regulation of gene expression and protein translation. In this review, we discuss recent findings regarding EMT-regulating ncRNAs and their associated signaling pathways involved in cancer progression.