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Up-regulation of LINC00467 promotes the tumourigenesis in colorectal cancer
Recent studies have reported that long non-coding RNAs (lncRNAs) are associated with the tumourigenesis of colorectal cancer (CRC); however, several of these are yet to be identified and characterised. In this study, we report a novel lncRNA, LINC00467, which was significantly up-regulated in CRC; w...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Ivyspring International Publisher
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6856745/ https://www.ncbi.nlm.nih.gov/pubmed/31772673 http://dx.doi.org/10.7150/jca.32216 |
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author | He, Xiaoyun Li, Shen Yu, Bingbing Kuang, Gaoyan Wu, Yongrong Zhang, Meili He, Yuxiang Ou, Chunlin Cao, Pengfei |
author_facet | He, Xiaoyun Li, Shen Yu, Bingbing Kuang, Gaoyan Wu, Yongrong Zhang, Meili He, Yuxiang Ou, Chunlin Cao, Pengfei |
author_sort | He, Xiaoyun |
collection | PubMed |
description | Recent studies have reported that long non-coding RNAs (lncRNAs) are associated with the tumourigenesis of colorectal cancer (CRC); however, several of these are yet to be identified and characterised. In this study, we report a novel lncRNA, LINC00467, which was significantly up-regulated in CRC; we investigated its function and mechanism in CRC. Our study demonstrated that LINC00467 levels in 45 pairs of CRC tissues were higher than those in the corresponding normal colon mucosal tissues. We used the Gene Expression Omnibus (GEO) and Gene Expression Profiling Interactive Analysis (GEPIA) databases for the analysis and measurement of clinical samples, and observed that the CRC patients with high LINC00467 expression levels showed poor overall survival (OS) and recurrent-free survival (RFS) rates. Furthermore, following the short interfering RNA (siRNA) knockdown of LINC00467 in the CRC cell line, the results demonstrated that LINC00467 suppresses the proliferation, invasion and metastasis of CRC cells in vitro. Moreover, its molecular mechanism of LINC00467 decreased the expression of Cyclin D1, Cyclin A1, CDK2, CDK4 and Twist1 as well as enhanced the expression of E‑cadherin. Collectively, these findings suggest that LINC00467 may be crucial in the progression and development of CRC, and may serve as a potential therapeutic target for CRC patients. |
format | Online Article Text |
id | pubmed-6856745 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Ivyspring International Publisher |
record_format | MEDLINE/PubMed |
spelling | pubmed-68567452019-11-26 Up-regulation of LINC00467 promotes the tumourigenesis in colorectal cancer He, Xiaoyun Li, Shen Yu, Bingbing Kuang, Gaoyan Wu, Yongrong Zhang, Meili He, Yuxiang Ou, Chunlin Cao, Pengfei J Cancer Research Paper Recent studies have reported that long non-coding RNAs (lncRNAs) are associated with the tumourigenesis of colorectal cancer (CRC); however, several of these are yet to be identified and characterised. In this study, we report a novel lncRNA, LINC00467, which was significantly up-regulated in CRC; we investigated its function and mechanism in CRC. Our study demonstrated that LINC00467 levels in 45 pairs of CRC tissues were higher than those in the corresponding normal colon mucosal tissues. We used the Gene Expression Omnibus (GEO) and Gene Expression Profiling Interactive Analysis (GEPIA) databases for the analysis and measurement of clinical samples, and observed that the CRC patients with high LINC00467 expression levels showed poor overall survival (OS) and recurrent-free survival (RFS) rates. Furthermore, following the short interfering RNA (siRNA) knockdown of LINC00467 in the CRC cell line, the results demonstrated that LINC00467 suppresses the proliferation, invasion and metastasis of CRC cells in vitro. Moreover, its molecular mechanism of LINC00467 decreased the expression of Cyclin D1, Cyclin A1, CDK2, CDK4 and Twist1 as well as enhanced the expression of E‑cadherin. Collectively, these findings suggest that LINC00467 may be crucial in the progression and development of CRC, and may serve as a potential therapeutic target for CRC patients. Ivyspring International Publisher 2019-10-19 /pmc/articles/PMC6856745/ /pubmed/31772673 http://dx.doi.org/10.7150/jca.32216 Text en © The author(s) This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions. |
spellingShingle | Research Paper He, Xiaoyun Li, Shen Yu, Bingbing Kuang, Gaoyan Wu, Yongrong Zhang, Meili He, Yuxiang Ou, Chunlin Cao, Pengfei Up-regulation of LINC00467 promotes the tumourigenesis in colorectal cancer |
title | Up-regulation of LINC00467 promotes the tumourigenesis in colorectal cancer |
title_full | Up-regulation of LINC00467 promotes the tumourigenesis in colorectal cancer |
title_fullStr | Up-regulation of LINC00467 promotes the tumourigenesis in colorectal cancer |
title_full_unstemmed | Up-regulation of LINC00467 promotes the tumourigenesis in colorectal cancer |
title_short | Up-regulation of LINC00467 promotes the tumourigenesis in colorectal cancer |
title_sort | up-regulation of linc00467 promotes the tumourigenesis in colorectal cancer |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6856745/ https://www.ncbi.nlm.nih.gov/pubmed/31772673 http://dx.doi.org/10.7150/jca.32216 |
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