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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...

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Autores principales: He, Xiaoyun, Li, Shen, Yu, Bingbing, Kuang, Gaoyan, Wu, Yongrong, Zhang, Meili, He, Yuxiang, Ou, Chunlin, Cao, Pengfei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2019
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.
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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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