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Long non‐coding RNA UCA1 contributes to the progression of oral squamous cell carcinoma by regulating the WNT/β‐catenin signaling pathway

With the development of functional genomics studies, a mass of long non‐coding RNAs (LncRNA) were discovered from the human genome. Long non‐coding RNAs serve as pivotal regulators of genes that are able to generate LncRNA–binding protein complexes to modulate a great number of genes. Recently, the...

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Autores principales: Yang, Yong‐Tao, Wang, Yu‐Fan, Lai, Ju‐Yi, Shen, Shi‐Yue, Wang, Feng, Kong, Jie, Zhang, Wei, Yang, Hong‐Yu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5132283/
https://www.ncbi.nlm.nih.gov/pubmed/27560546
http://dx.doi.org/10.1111/cas.13058
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author Yang, Yong‐Tao
Wang, Yu‐Fan
Lai, Ju‐Yi
Shen, Shi‐Yue
Wang, Feng
Kong, Jie
Zhang, Wei
Yang, Hong‐Yu
author_facet Yang, Yong‐Tao
Wang, Yu‐Fan
Lai, Ju‐Yi
Shen, Shi‐Yue
Wang, Feng
Kong, Jie
Zhang, Wei
Yang, Hong‐Yu
author_sort Yang, Yong‐Tao
collection PubMed
description With the development of functional genomics studies, a mass of long non‐coding RNAs (LncRNA) were discovered from the human genome. Long non‐coding RNAs serve as pivotal regulators of genes that are able to generate LncRNA–binding protein complexes to modulate a great number of genes. Recently, the LncRNA urothelial carcinoma‐associated 1 (UCA1) has been revealed to be dysregulated, which plays a critical role in the development of a few cancers. However, the role of the biology and clinical significance of UCA1 in the tumorigenesis of oral squamous cell carcinoma (OSCC) remain unknown. We found that UCA1 expression levels were upregulated aberrantly in tongue squamous cell carcinoma tissues and associated with lymph node metastasis and TNM stage. We explored the expression, function, and molecular mechanism of LncRNA UCA1 in OSCC. In the present work, we revealed that UCA1 silencing suppressed proliferation and metastasis and induced apoptosis of OSCC cell lines in vitro and in vivo, which might be related to the activation level of the WNT/β‐catenin signaling pathway. Our research results emphasize the pivotal role of UCA1 in the oncogenesis of OSCC and reveal a novel LncRNA UCA1–β‐catenin–WNT signaling pathway regulatory network that could contribute to our understanding in the pathogenesis of OSCC and assist in the discovery of a viable LncRNA‐directed diagnostic and therapeutic strategy for this fatal disease.
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spelling pubmed-51322832016-12-15 Long non‐coding RNA UCA1 contributes to the progression of oral squamous cell carcinoma by regulating the WNT/β‐catenin signaling pathway Yang, Yong‐Tao Wang, Yu‐Fan Lai, Ju‐Yi Shen, Shi‐Yue Wang, Feng Kong, Jie Zhang, Wei Yang, Hong‐Yu Cancer Sci Original Articles With the development of functional genomics studies, a mass of long non‐coding RNAs (LncRNA) were discovered from the human genome. Long non‐coding RNAs serve as pivotal regulators of genes that are able to generate LncRNA–binding protein complexes to modulate a great number of genes. Recently, the LncRNA urothelial carcinoma‐associated 1 (UCA1) has been revealed to be dysregulated, which plays a critical role in the development of a few cancers. However, the role of the biology and clinical significance of UCA1 in the tumorigenesis of oral squamous cell carcinoma (OSCC) remain unknown. We found that UCA1 expression levels were upregulated aberrantly in tongue squamous cell carcinoma tissues and associated with lymph node metastasis and TNM stage. We explored the expression, function, and molecular mechanism of LncRNA UCA1 in OSCC. In the present work, we revealed that UCA1 silencing suppressed proliferation and metastasis and induced apoptosis of OSCC cell lines in vitro and in vivo, which might be related to the activation level of the WNT/β‐catenin signaling pathway. Our research results emphasize the pivotal role of UCA1 in the oncogenesis of OSCC and reveal a novel LncRNA UCA1–β‐catenin–WNT signaling pathway regulatory network that could contribute to our understanding in the pathogenesis of OSCC and assist in the discovery of a viable LncRNA‐directed diagnostic and therapeutic strategy for this fatal disease. John Wiley and Sons Inc. 2016-11-04 2016-11 /pmc/articles/PMC5132283/ /pubmed/27560546 http://dx.doi.org/10.1111/cas.13058 Text en © 2016 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs (http://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Original Articles
Yang, Yong‐Tao
Wang, Yu‐Fan
Lai, Ju‐Yi
Shen, Shi‐Yue
Wang, Feng
Kong, Jie
Zhang, Wei
Yang, Hong‐Yu
Long non‐coding RNA UCA1 contributes to the progression of oral squamous cell carcinoma by regulating the WNT/β‐catenin signaling pathway
title Long non‐coding RNA UCA1 contributes to the progression of oral squamous cell carcinoma by regulating the WNT/β‐catenin signaling pathway
title_full Long non‐coding RNA UCA1 contributes to the progression of oral squamous cell carcinoma by regulating the WNT/β‐catenin signaling pathway
title_fullStr Long non‐coding RNA UCA1 contributes to the progression of oral squamous cell carcinoma by regulating the WNT/β‐catenin signaling pathway
title_full_unstemmed Long non‐coding RNA UCA1 contributes to the progression of oral squamous cell carcinoma by regulating the WNT/β‐catenin signaling pathway
title_short Long non‐coding RNA UCA1 contributes to the progression of oral squamous cell carcinoma by regulating the WNT/β‐catenin signaling pathway
title_sort long non‐coding rna uca1 contributes to the progression of oral squamous cell carcinoma by regulating the wnt/β‐catenin signaling pathway
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5132283/
https://www.ncbi.nlm.nih.gov/pubmed/27560546
http://dx.doi.org/10.1111/cas.13058
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