Noncoding RNAs in Tumor Epithelial-to-Mesenchymal Transition

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 epi...

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Published inStem cells international Vol. 2016; no. 2016; pp. 1 - 13
Main Authors Lin, Ching-Wen, Yang, Pan-Chyr, Lin, Pei-Ying
Format Journal Article
LanguageEnglish
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
Online AccessGet full text
ISSN1687-966X
1687-9678
1687-9678
DOI10.1155/2016/2732705

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Abstract 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.
AbstractList 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.
Audience Academic
Author Lin, Ching-Wen
Lin, Pei-Ying
Yang, Pan-Chyr
AuthorAffiliation 2 National Center of Excellence for Clinical Trials and Research Center, Department of Medical Research, National Taiwan University Hospital, Taipei 10043, Taiwan
3 Department of Internal Medicine, National Taiwan University Hospital and College of Medicine, National Taiwan University, Taipei 70101, Taiwan
1 Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan
AuthorAffiliation_xml – name: 2 National Center of Excellence for Clinical Trials and Research Center, Department of Medical Research, National Taiwan University Hospital, Taipei 10043, Taiwan
– name: 3 Department of Internal Medicine, National Taiwan University Hospital and College of Medicine, National Taiwan University, Taipei 70101, Taiwan
– name: 1 Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/26989421$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright Copyright © 2016 Ching-Wen Lin et al.
COPYRIGHT 2016 John Wiley & Sons, Inc.
Copyright © 2016 Ching-Wen Lin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Copyright © 2016 Ching-Wen Lin et al. 2016
Copyright_xml – notice: Copyright © 2016 Ching-Wen Lin et al.
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– notice: Copyright © 2016 Ching-Wen Lin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
– notice: Copyright © 2016 Ching-Wen Lin et al. 2016
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Snippet Epithelial-derived tumor cells acquire the capacity for epithelial-to-mesenchymal transition (EMT), which enables them to invade adjacent tissues and/or...
Epithelial‐derived tumor cells acquire the capacity for epithelial‐to‐mesenchymal transition (EMT), which enables them to invade adjacent tissues and/or...
Epithelial-derived tumor cells acquire the capacity for epithelial-to -mesenchymal transition (EMT), which enables them to invade adjacent tissues and/or...
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StartPage 1
SubjectTerms 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
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Title Noncoding RNAs in Tumor Epithelial-to-Mesenchymal Transition
URI https://search.emarefa.net/detail/BIM-1116300
https://dx.doi.org/10.1155/2016/2732705
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