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lncRNA VIM-AS1 promotes cell proliferation, metastasis and epithelial-mesenchymal transition by activating the Wnt/β-catenin pathway in gastric cancer

The present study aimed to explore the biological functions and molecular mechanisms of the long non-coding RNA VIM antisense RNA 1 (VIM-AS1) in gastric cancer (GC). The expression of VIM-AS1 was analyzed in tissues from patients with GC and GC cell lines by reverse transcription-quantitative (RT-q)...

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Autores principales: Sun, Jin-Gui, Li, Xiao-Bo, Yin, Rui-Hong, Li, Xiao-Feng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7646824/
https://www.ncbi.nlm.nih.gov/pubmed/33173977
http://dx.doi.org/10.3892/mmr.2020.11577
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author Sun, Jin-Gui
Li, Xiao-Bo
Yin, Rui-Hong
Li, Xiao-Feng
author_facet Sun, Jin-Gui
Li, Xiao-Bo
Yin, Rui-Hong
Li, Xiao-Feng
author_sort Sun, Jin-Gui
collection PubMed
description The present study aimed to explore the biological functions and molecular mechanisms of the long non-coding RNA VIM antisense RNA 1 (VIM-AS1) in gastric cancer (GC). The expression of VIM-AS1 was analyzed in tissues from patients with GC and GC cell lines by reverse transcription-quantitative (RT-q)PCR. The relationship between VIM-AS1 expression and overall survival time of patients with GC was also assessed. To determine the biological functions of VIM-AS1, Cell Counting Kit-8 assay, colony formation assay, flow cytometry, wound healing assay and Transwell assay were employed. The targeting relationship among VIM-AS1, microRNA (miR)-8052 and frizzled 1 (FZD1) was verified by the dual luciferase reporter gene assay. The underlying molecular mechanism of VIM-AS1 on GC was determined by RT-qPCR and western blotting. In addition, tumor formation was detected in nude mice. The results of the present study demonstrated that VIM-AS1 was highly expressed in GC tissues and cells. In addition, VIM-AS1 expression was demonstrated to be closely related to the prognosis of patients with GC. Notably, silencing VIM-AS1 inhibited the proliferation, migration and invasion, and enhanced apoptosis of AGS and HGC-27 cells. Silencing VIM-AS1 significantly increased the protein expression levels of cleaved caspase-3, Bax and E-cadherin, but decreased the protein expression levels of Bcl-2, N-cadherin, vimentin, matrix metalloproteinase (MMP)-2, MMP-9, β-catenin, cyclin D1, C-myc and FZD1. Additionally, silencing VIM-AS1 inhibited tumor growth in nude mice. Cumulatively, the present study demonstrated that VIM-AS1 may promote cell proliferation, migration, invasion and epithelial-mesenchymal transition by regulating FDZ1 and activating the Wnt/β-catenin pathway in GC.
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spelling pubmed-76468242020-11-13 lncRNA VIM-AS1 promotes cell proliferation, metastasis and epithelial-mesenchymal transition by activating the Wnt/β-catenin pathway in gastric cancer Sun, Jin-Gui Li, Xiao-Bo Yin, Rui-Hong Li, Xiao-Feng Mol Med Rep Articles The present study aimed to explore the biological functions and molecular mechanisms of the long non-coding RNA VIM antisense RNA 1 (VIM-AS1) in gastric cancer (GC). The expression of VIM-AS1 was analyzed in tissues from patients with GC and GC cell lines by reverse transcription-quantitative (RT-q)PCR. The relationship between VIM-AS1 expression and overall survival time of patients with GC was also assessed. To determine the biological functions of VIM-AS1, Cell Counting Kit-8 assay, colony formation assay, flow cytometry, wound healing assay and Transwell assay were employed. The targeting relationship among VIM-AS1, microRNA (miR)-8052 and frizzled 1 (FZD1) was verified by the dual luciferase reporter gene assay. The underlying molecular mechanism of VIM-AS1 on GC was determined by RT-qPCR and western blotting. In addition, tumor formation was detected in nude mice. The results of the present study demonstrated that VIM-AS1 was highly expressed in GC tissues and cells. In addition, VIM-AS1 expression was demonstrated to be closely related to the prognosis of patients with GC. Notably, silencing VIM-AS1 inhibited the proliferation, migration and invasion, and enhanced apoptosis of AGS and HGC-27 cells. Silencing VIM-AS1 significantly increased the protein expression levels of cleaved caspase-3, Bax and E-cadherin, but decreased the protein expression levels of Bcl-2, N-cadherin, vimentin, matrix metalloproteinase (MMP)-2, MMP-9, β-catenin, cyclin D1, C-myc and FZD1. Additionally, silencing VIM-AS1 inhibited tumor growth in nude mice. Cumulatively, the present study demonstrated that VIM-AS1 may promote cell proliferation, migration, invasion and epithelial-mesenchymal transition by regulating FDZ1 and activating the Wnt/β-catenin pathway in GC. D.A. Spandidos 2020-12 2020-10-11 /pmc/articles/PMC7646824/ /pubmed/33173977 http://dx.doi.org/10.3892/mmr.2020.11577 Text en Copyright: © Sun et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Sun, Jin-Gui
Li, Xiao-Bo
Yin, Rui-Hong
Li, Xiao-Feng
lncRNA VIM-AS1 promotes cell proliferation, metastasis and epithelial-mesenchymal transition by activating the Wnt/β-catenin pathway in gastric cancer
title lncRNA VIM-AS1 promotes cell proliferation, metastasis and epithelial-mesenchymal transition by activating the Wnt/β-catenin pathway in gastric cancer
title_full lncRNA VIM-AS1 promotes cell proliferation, metastasis and epithelial-mesenchymal transition by activating the Wnt/β-catenin pathway in gastric cancer
title_fullStr lncRNA VIM-AS1 promotes cell proliferation, metastasis and epithelial-mesenchymal transition by activating the Wnt/β-catenin pathway in gastric cancer
title_full_unstemmed lncRNA VIM-AS1 promotes cell proliferation, metastasis and epithelial-mesenchymal transition by activating the Wnt/β-catenin pathway in gastric cancer
title_short lncRNA VIM-AS1 promotes cell proliferation, metastasis and epithelial-mesenchymal transition by activating the Wnt/β-catenin pathway in gastric cancer
title_sort lncrna vim-as1 promotes cell proliferation, metastasis and epithelial-mesenchymal transition by activating the wnt/β-catenin pathway in gastric cancer
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7646824/
https://www.ncbi.nlm.nih.gov/pubmed/33173977
http://dx.doi.org/10.3892/mmr.2020.11577
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