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Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer
Long intergenic noncoding RNAs (lincRNAs) have important roles in biological functions, molecular mechanisms and prognostic values in colorectal cancer (CRC). In this context, the roles of linc-UFC1 remain to be elucidated. In this study, linc-UFC1 was overexpressed in CRC patient tissues and positi...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4917661/ https://www.ncbi.nlm.nih.gov/pubmed/27195675 http://dx.doi.org/10.1038/cddis.2016.124 |
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author | Yu, T Shan, T-D Li, J-Y Huang, C-Z Wang, S-Y Ouyang, H Lu, X-J Xu, J-H Zhong, W Chen, Q-K |
author_facet | Yu, T Shan, T-D Li, J-Y Huang, C-Z Wang, S-Y Ouyang, H Lu, X-J Xu, J-H Zhong, W Chen, Q-K |
author_sort | Yu, T |
collection | PubMed |
description | Long intergenic noncoding RNAs (lincRNAs) have important roles in biological functions, molecular mechanisms and prognostic values in colorectal cancer (CRC). In this context, the roles of linc-UFC1 remain to be elucidated. In this study, linc-UFC1 was overexpressed in CRC patient tissues and positively correlated with tumor grade, N stage and M stage. Inhibition of linc-UFC1 resulted in cell proliferation inhibition and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, Rb and phosphorylated Rb. In addition, inhibition of linc-UFC1 induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-9 and caspase-3. An investigation of the signaling pathway revealed that the effects on proliferation and apoptosis following linc-UFC1 knockdown were mediated by suppression of β-catenin and activation of phosphorylated P38. Furthermore, the P38 inhibitor SB203580 could attenuate the apoptotic effect achieved by linc-UFC1 knockdown, confirming the involvement of P38 signaling in the induced apoptosis. Taken together, linc-UFC1 might have a critical role in pro-proliferation and anti-apoptosis in CRC by regulating the cell cycle, intrinsic apoptosis, and β-catenin and P38 signaling. Thus, linc-UFC1 could be a potential therapeutic target and novel molecular biomarker for CRC. |
format | Online Article Text |
id | pubmed-4917661 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-49176612016-07-07 Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer Yu, T Shan, T-D Li, J-Y Huang, C-Z Wang, S-Y Ouyang, H Lu, X-J Xu, J-H Zhong, W Chen, Q-K Cell Death Dis Original Article Long intergenic noncoding RNAs (lincRNAs) have important roles in biological functions, molecular mechanisms and prognostic values in colorectal cancer (CRC). In this context, the roles of linc-UFC1 remain to be elucidated. In this study, linc-UFC1 was overexpressed in CRC patient tissues and positively correlated with tumor grade, N stage and M stage. Inhibition of linc-UFC1 resulted in cell proliferation inhibition and G1 cell cycle arrest, which was mediated by cyclin D1, CDK4, Rb and phosphorylated Rb. In addition, inhibition of linc-UFC1 induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-9 and caspase-3. An investigation of the signaling pathway revealed that the effects on proliferation and apoptosis following linc-UFC1 knockdown were mediated by suppression of β-catenin and activation of phosphorylated P38. Furthermore, the P38 inhibitor SB203580 could attenuate the apoptotic effect achieved by linc-UFC1 knockdown, confirming the involvement of P38 signaling in the induced apoptosis. Taken together, linc-UFC1 might have a critical role in pro-proliferation and anti-apoptosis in CRC by regulating the cell cycle, intrinsic apoptosis, and β-catenin and P38 signaling. Thus, linc-UFC1 could be a potential therapeutic target and novel molecular biomarker for CRC. Nature Publishing Group 2016-05 2016-05-19 /pmc/articles/PMC4917661/ /pubmed/27195675 http://dx.doi.org/10.1038/cddis.2016.124 Text en Copyright © 2016 Macmillan Publishers Limited 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 Yu, T Shan, T-D Li, J-Y Huang, C-Z Wang, S-Y Ouyang, H Lu, X-J Xu, J-H Zhong, W Chen, Q-K Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer |
title | Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer |
title_full | Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer |
title_fullStr | Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer |
title_full_unstemmed | Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer |
title_short | Knockdown of linc-UFC1 suppresses proliferation and induces apoptosis of colorectal cancer |
title_sort | knockdown of linc-ufc1 suppresses proliferation and induces apoptosis of colorectal cancer |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4917661/ https://www.ncbi.nlm.nih.gov/pubmed/27195675 http://dx.doi.org/10.1038/cddis.2016.124 |
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