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The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143
The human genome contains thousands of long intergenic noncoding RNAs (lincRNAs). However, the functional roles of these transcripts and the mechanisms responsible for their deregulation in colorectal cancer (CRC) remain elusive. A novel lincRNA termed upregulated in CRC (UCC) was found to be highly...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5520712/ https://www.ncbi.nlm.nih.gov/pubmed/28492554 http://dx.doi.org/10.1038/cddis.2017.191 |
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author | Huang, Feng-Ting Chen, Wen-Ying Gu, Zhi-Qiang Zhuang, Yan-Yan Li, Chu-Qiang Wang, Ling-Yun Peng, Juan-Fei Zhu, Zhe Luo, Xin Li, Yuan-Hua Yao, He-Rui Zhang, Shi-Neng |
author_facet | Huang, Feng-Ting Chen, Wen-Ying Gu, Zhi-Qiang Zhuang, Yan-Yan Li, Chu-Qiang Wang, Ling-Yun Peng, Juan-Fei Zhu, Zhe Luo, Xin Li, Yuan-Hua Yao, He-Rui Zhang, Shi-Neng |
author_sort | Huang, Feng-Ting |
collection | PubMed |
description | The human genome contains thousands of long intergenic noncoding RNAs (lincRNAs). However, the functional roles of these transcripts and the mechanisms responsible for their deregulation in colorectal cancer (CRC) remain elusive. A novel lincRNA termed upregulated in CRC (UCC) was found to be highly expressed in human CRC tissues and cell lines. UCC levels correlated with lymph node metastasis, Dukes’ stage, and patient outcomes. In SW480 and SW620 cells, knockdown of UCC inhibited proliferation, invasion, and cell cycle progression and induced apoptosis in vitro. Xenograft tumors grown from UCC-silenced SW620 cells had smaller mean volumes and formed more slowly than xenograft tumors grown from control cells. Inversely, overexpression of UCC in HCT116 promoted cell growth and invasion in vitro. Bioinformatics analysis, dual-luciferase reporter assays, and RNA immunoprecipitation assays showed that miR-143 can interact with UCC, and we found that UCC expression inversely correlates with miR-143 expression in CRC specimens. Moreover, mechanistic investigations showed that UCC may act as an endogenous sponge by competing for miR-143, thereby regulating the targets of this miRNA. Our results suggest that UCC and miR-143 may be promising molecular targets for CRC therapy. |
format | Online Article Text |
id | pubmed-5520712 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-55207122017-07-27 The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143 Huang, Feng-Ting Chen, Wen-Ying Gu, Zhi-Qiang Zhuang, Yan-Yan Li, Chu-Qiang Wang, Ling-Yun Peng, Juan-Fei Zhu, Zhe Luo, Xin Li, Yuan-Hua Yao, He-Rui Zhang, Shi-Neng Cell Death Dis Original Article The human genome contains thousands of long intergenic noncoding RNAs (lincRNAs). However, the functional roles of these transcripts and the mechanisms responsible for their deregulation in colorectal cancer (CRC) remain elusive. A novel lincRNA termed upregulated in CRC (UCC) was found to be highly expressed in human CRC tissues and cell lines. UCC levels correlated with lymph node metastasis, Dukes’ stage, and patient outcomes. In SW480 and SW620 cells, knockdown of UCC inhibited proliferation, invasion, and cell cycle progression and induced apoptosis in vitro. Xenograft tumors grown from UCC-silenced SW620 cells had smaller mean volumes and formed more slowly than xenograft tumors grown from control cells. Inversely, overexpression of UCC in HCT116 promoted cell growth and invasion in vitro. Bioinformatics analysis, dual-luciferase reporter assays, and RNA immunoprecipitation assays showed that miR-143 can interact with UCC, and we found that UCC expression inversely correlates with miR-143 expression in CRC specimens. Moreover, mechanistic investigations showed that UCC may act as an endogenous sponge by competing for miR-143, thereby regulating the targets of this miRNA. Our results suggest that UCC and miR-143 may be promising molecular targets for CRC therapy. Nature Publishing Group 2017-05-11 /pmc/articles/PMC5520712/ /pubmed/28492554 http://dx.doi.org/10.1038/cddis.2017.191 Text en Copyright © 2017 The Author(s) http://creativecommons.org/licenses/by/4.0/ Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Original Article Huang, Feng-Ting Chen, Wen-Ying Gu, Zhi-Qiang Zhuang, Yan-Yan Li, Chu-Qiang Wang, Ling-Yun Peng, Juan-Fei Zhu, Zhe Luo, Xin Li, Yuan-Hua Yao, He-Rui Zhang, Shi-Neng The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143 |
title | The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143 |
title_full | The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143 |
title_fullStr | The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143 |
title_full_unstemmed | The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143 |
title_short | The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143 |
title_sort | novel long intergenic noncoding rna ucc promotes colorectal cancer progression by sponging mir-143 |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5520712/ https://www.ncbi.nlm.nih.gov/pubmed/28492554 http://dx.doi.org/10.1038/cddis.2017.191 |
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