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Long noncoding RNA RP4 functions as a competing endogenous RNA through miR-7-5p sponge activity in colorectal cancer
AIM: To investigate the role of long noncoding RNA (lncRNA) RP4 in colorectal cancer. METHODS: Lentivirus-mediated lncRNA RP4 overexpression and knockdown were performed in the colorectal cancer cell line SW480. Cell proliferation, tumor growth, and early apoptosis were evaluated by a cell counting...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Baishideng Publishing Group Inc
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5840465/ https://www.ncbi.nlm.nih.gov/pubmed/29531464 http://dx.doi.org/10.3748/wjg.v24.i9.1004 |
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author | Liu, Mu-Lin Zhang, Qiao Yuan, Xiao Jin, Long Wang, Li-Li Fang, Tao-Tao Wang, Wen-Bin |
author_facet | Liu, Mu-Lin Zhang, Qiao Yuan, Xiao Jin, Long Wang, Li-Li Fang, Tao-Tao Wang, Wen-Bin |
author_sort | Liu, Mu-Lin |
collection | PubMed |
description | AIM: To investigate the role of long noncoding RNA (lncRNA) RP4 in colorectal cancer. METHODS: Lentivirus-mediated lncRNA RP4 overexpression and knockdown were performed in the colorectal cancer cell line SW480. Cell proliferation, tumor growth, and early apoptosis were evaluated by a cell counting kit-8 assay, an in vivo xenograft tumor model, and annexin V/propidium iodide staining, respectively. Analysis of the lncRNA RP4 mechanism involved assessment of the association of its expression with miR-7-5p and the SH3GLB1 gene. Western blot analysis was also performed to assess the effect of lncRNA RP4 on the autophagy-mediated cell death pathway and phosphatidylinositol-3-kinase (PI3K)/Akt signaling. RESULTS: Cell proliferation, tumor growth, and early apoptosis in SW480 cells were negatively regulated by lncRNA RP4. Functional experiments indicated that lncRNA RP4 directly upregulated SH3GLB1 expression by acting as a competing endogenous RNA (ceRNA) for miR-7-5p. This interaction led to activation of the autophagy-mediated cell death pathway and de-repression of PI3K and Akt phosphorylation in colorectal cancer cells in vivo. CONCLUSION: Our results demonstrated that lncRNA RP4 is a ceRNA that plays an important role in the pathogenesis of colorectal cancer, and could be a potential therapeutic target for colorectal cancer treatment. |
format | Online Article Text |
id | pubmed-5840465 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Baishideng Publishing Group Inc |
record_format | MEDLINE/PubMed |
spelling | pubmed-58404652018-03-12 Long noncoding RNA RP4 functions as a competing endogenous RNA through miR-7-5p sponge activity in colorectal cancer Liu, Mu-Lin Zhang, Qiao Yuan, Xiao Jin, Long Wang, Li-Li Fang, Tao-Tao Wang, Wen-Bin World J Gastroenterol Basic Study AIM: To investigate the role of long noncoding RNA (lncRNA) RP4 in colorectal cancer. METHODS: Lentivirus-mediated lncRNA RP4 overexpression and knockdown were performed in the colorectal cancer cell line SW480. Cell proliferation, tumor growth, and early apoptosis were evaluated by a cell counting kit-8 assay, an in vivo xenograft tumor model, and annexin V/propidium iodide staining, respectively. Analysis of the lncRNA RP4 mechanism involved assessment of the association of its expression with miR-7-5p and the SH3GLB1 gene. Western blot analysis was also performed to assess the effect of lncRNA RP4 on the autophagy-mediated cell death pathway and phosphatidylinositol-3-kinase (PI3K)/Akt signaling. RESULTS: Cell proliferation, tumor growth, and early apoptosis in SW480 cells were negatively regulated by lncRNA RP4. Functional experiments indicated that lncRNA RP4 directly upregulated SH3GLB1 expression by acting as a competing endogenous RNA (ceRNA) for miR-7-5p. This interaction led to activation of the autophagy-mediated cell death pathway and de-repression of PI3K and Akt phosphorylation in colorectal cancer cells in vivo. CONCLUSION: Our results demonstrated that lncRNA RP4 is a ceRNA that plays an important role in the pathogenesis of colorectal cancer, and could be a potential therapeutic target for colorectal cancer treatment. Baishideng Publishing Group Inc 2018-03-07 2018-03-07 /pmc/articles/PMC5840465/ /pubmed/29531464 http://dx.doi.org/10.3748/wjg.v24.i9.1004 Text en ©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved. http://creativecommons.org/licenses/by-nc/4.0/ This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. |
spellingShingle | Basic Study Liu, Mu-Lin Zhang, Qiao Yuan, Xiao Jin, Long Wang, Li-Li Fang, Tao-Tao Wang, Wen-Bin Long noncoding RNA RP4 functions as a competing endogenous RNA through miR-7-5p sponge activity in colorectal cancer |
title | Long noncoding RNA RP4 functions as a competing endogenous RNA through miR-7-5p sponge activity in colorectal cancer |
title_full | Long noncoding RNA RP4 functions as a competing endogenous RNA through miR-7-5p sponge activity in colorectal cancer |
title_fullStr | Long noncoding RNA RP4 functions as a competing endogenous RNA through miR-7-5p sponge activity in colorectal cancer |
title_full_unstemmed | Long noncoding RNA RP4 functions as a competing endogenous RNA through miR-7-5p sponge activity in colorectal cancer |
title_short | Long noncoding RNA RP4 functions as a competing endogenous RNA through miR-7-5p sponge activity in colorectal cancer |
title_sort | long noncoding rna rp4 functions as a competing endogenous rna through mir-7-5p sponge activity in colorectal cancer |
topic | Basic Study |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5840465/ https://www.ncbi.nlm.nih.gov/pubmed/29531464 http://dx.doi.org/10.3748/wjg.v24.i9.1004 |
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