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LncRNA NEAT1 promotes the tumorigenesis of colorectal cancer by sponging miR‐193a‐3p
OBJECTIVES: LncRNA nuclear‐enriched abundant transcript 1 (NEAT1) participates in the development and progression of multiple malignancies. However, the molecular mechanism by which NEAT1 contributes to colorectal cancer (CRC) remains unclear. METHODS: The association between lncRNA NEAT1 expression...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6430453/ https://www.ncbi.nlm.nih.gov/pubmed/30407674 http://dx.doi.org/10.1111/cpr.12526 |
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author | Yu, Hong‐Mei Wang, Chen Yuan, Zhen Chen, Guang‐Liang Ye, Tao Yang, Bi‐Wei |
author_facet | Yu, Hong‐Mei Wang, Chen Yuan, Zhen Chen, Guang‐Liang Ye, Tao Yang, Bi‐Wei |
author_sort | Yu, Hong‐Mei |
collection | PubMed |
description | OBJECTIVES: LncRNA nuclear‐enriched abundant transcript 1 (NEAT1) participates in the development and progression of multiple malignancies. However, the molecular mechanism by which NEAT1 contributes to colorectal cancer (CRC) remains unclear. METHODS: The association between lncRNA NEAT1 expression and clinicopathological characteristics and prognosis in patients with CRC was analysed by TCGA RNA‐sequencing data. MTT, colony formation, flow cytometry, transwell assays and a xenograft tumour model were used to assess the functions of NEAT1. Bioinformatics and spearman correlation analysis were used to identify the NEAT1‐specific binding with miRNAs, and luciferase gene report and RIP assays were performed to confirm the interaction between miR‐193a‐3p (miR‐193a) and NEAT1 in CRC cells. RESULTS: Upregulation of NEAT1 expression was significantly correlated with TNM stage, poor survival and tumour recurrence in patients with CRC, and acted as an independent prognostic factor for tumour recurrence. Knockdown of NEAT1 suppressed cell proliferation, colony formation abilities and invasive potential and induced cell apoptosis, but overexpression of NEAT1 reversed these effects. Furthermore, NEAT1 was confirmed to act as a sponge of miR‐193a, and knockdown of NEAT1 attenuated miR‐193a inhibitor‐induced tumour promoting effects and L17RD expression in CRC cells. miR‐193a harboured negative correlation with NEAT1 and IL17RD expression in CRC specimens. In vivo experiment further validated the inhibitory effects of NEAT1 knockdown on xenograft tumour growth. CONCLUSION: Our findings demonstrate that lncRNA NEAT1 acts as an oncogenic role in CRC cells by sponging miR‐193a and may represent a potential marker for CRC patients. |
format | Online Article Text |
id | pubmed-6430453 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-64304532020-03-13 LncRNA NEAT1 promotes the tumorigenesis of colorectal cancer by sponging miR‐193a‐3p Yu, Hong‐Mei Wang, Chen Yuan, Zhen Chen, Guang‐Liang Ye, Tao Yang, Bi‐Wei Cell Prolif Original Articles OBJECTIVES: LncRNA nuclear‐enriched abundant transcript 1 (NEAT1) participates in the development and progression of multiple malignancies. However, the molecular mechanism by which NEAT1 contributes to colorectal cancer (CRC) remains unclear. METHODS: The association between lncRNA NEAT1 expression and clinicopathological characteristics and prognosis in patients with CRC was analysed by TCGA RNA‐sequencing data. MTT, colony formation, flow cytometry, transwell assays and a xenograft tumour model were used to assess the functions of NEAT1. Bioinformatics and spearman correlation analysis were used to identify the NEAT1‐specific binding with miRNAs, and luciferase gene report and RIP assays were performed to confirm the interaction between miR‐193a‐3p (miR‐193a) and NEAT1 in CRC cells. RESULTS: Upregulation of NEAT1 expression was significantly correlated with TNM stage, poor survival and tumour recurrence in patients with CRC, and acted as an independent prognostic factor for tumour recurrence. Knockdown of NEAT1 suppressed cell proliferation, colony formation abilities and invasive potential and induced cell apoptosis, but overexpression of NEAT1 reversed these effects. Furthermore, NEAT1 was confirmed to act as a sponge of miR‐193a, and knockdown of NEAT1 attenuated miR‐193a inhibitor‐induced tumour promoting effects and L17RD expression in CRC cells. miR‐193a harboured negative correlation with NEAT1 and IL17RD expression in CRC specimens. In vivo experiment further validated the inhibitory effects of NEAT1 knockdown on xenograft tumour growth. CONCLUSION: Our findings demonstrate that lncRNA NEAT1 acts as an oncogenic role in CRC cells by sponging miR‐193a and may represent a potential marker for CRC patients. John Wiley and Sons Inc. 2018-11-08 /pmc/articles/PMC6430453/ /pubmed/30407674 http://dx.doi.org/10.1111/cpr.12526 Text en © 2018 The Authors Cell Proliferation Published by John Wiley & Sons Ltd This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Yu, Hong‐Mei Wang, Chen Yuan, Zhen Chen, Guang‐Liang Ye, Tao Yang, Bi‐Wei LncRNA NEAT1 promotes the tumorigenesis of colorectal cancer by sponging miR‐193a‐3p |
title | LncRNA NEAT1 promotes the tumorigenesis of colorectal cancer by sponging miR‐193a‐3p |
title_full | LncRNA NEAT1 promotes the tumorigenesis of colorectal cancer by sponging miR‐193a‐3p |
title_fullStr | LncRNA NEAT1 promotes the tumorigenesis of colorectal cancer by sponging miR‐193a‐3p |
title_full_unstemmed | LncRNA NEAT1 promotes the tumorigenesis of colorectal cancer by sponging miR‐193a‐3p |
title_short | LncRNA NEAT1 promotes the tumorigenesis of colorectal cancer by sponging miR‐193a‐3p |
title_sort | lncrna neat1 promotes the tumorigenesis of colorectal cancer by sponging mir‐193a‐3p |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6430453/ https://www.ncbi.nlm.nih.gov/pubmed/30407674 http://dx.doi.org/10.1111/cpr.12526 |
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