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Overexpression of Long Non-Coding RNA TUG1 Promotes Colon Cancer Progression
BACKGROUND: Colon cancer is one of the most prevalent and deadly cancers worldwide. It is still necessary to further define the mechanisms and explore therapeutic targets of colon cancer. Dysregulation of long noncoding RNAs (lncRNAs) has been shown to be correlated with diverse biological processes...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5027858/ https://www.ncbi.nlm.nih.gov/pubmed/27634385 http://dx.doi.org/10.12659/MSM.897072 |
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author | Zhai, Hui-yuan Sui, Ming-hua Yu, Xiao Qu, Zhen Hu, Jin-chen Sun, Hai-qing Zheng, Hai-tao Zhou, Kai Jiang, Li-xin |
author_facet | Zhai, Hui-yuan Sui, Ming-hua Yu, Xiao Qu, Zhen Hu, Jin-chen Sun, Hai-qing Zheng, Hai-tao Zhou, Kai Jiang, Li-xin |
author_sort | Zhai, Hui-yuan |
collection | PubMed |
description | BACKGROUND: Colon cancer is one of the most prevalent and deadly cancers worldwide. It is still necessary to further define the mechanisms and explore therapeutic targets of colon cancer. Dysregulation of long noncoding RNAs (lncRNAs) has been shown to be correlated with diverse biological processes, including tumorigenesis. This study aimed to characterize the biological mechanism of taurine-upregulated gene 1 (TUG1) in colon cancer. MATERIAL/METHODS: qRT-PCR was used to analyze the expression level of TUG1 and p63 in 75 colon cancer tissues and the matched adjacent non-tumor tissue. In vitro, cultured colon cancer cell lines HCT-116 and LoVo were used as cell models. TUG1 and p63 were silenced via transferring siRNA into HCT-116 or LoVo. The effects of TUG1 were investigated by examining cell proliferation, apoptosis, and migration. RESULTS: Among the 75 colon cancer cases, the expression of TUG1 was significantly higher in colon cancer tissues compared with the matched adjacent non-tumor tissue, while p63 expression was lower in the tumor tissue. In HCT-116 and LoVo, the expression of TUG1 was significantly increased by p63 siRNA transfection. Furthermore, down-regulation of TUG1 by siRNA significantly inhibited the cell proliferation and promoted colon cancer cell apoptosis. In addition, inhibition of TUG1 expression significantly blocked the cell migration ability of colon cancer cells. CONCLUSIONS: LncRNA TUG1 may serve as a potential oncogene for colon cancer. Overexpressed TUG1 may contribute to promoting cell proliferation and migration in colon cancer cells. |
format | Online Article Text |
id | pubmed-5027858 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | International Scientific Literature, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-50278582016-09-29 Overexpression of Long Non-Coding RNA TUG1 Promotes Colon Cancer Progression Zhai, Hui-yuan Sui, Ming-hua Yu, Xiao Qu, Zhen Hu, Jin-chen Sun, Hai-qing Zheng, Hai-tao Zhou, Kai Jiang, Li-xin Med Sci Monit Molecular Biology BACKGROUND: Colon cancer is one of the most prevalent and deadly cancers worldwide. It is still necessary to further define the mechanisms and explore therapeutic targets of colon cancer. Dysregulation of long noncoding RNAs (lncRNAs) has been shown to be correlated with diverse biological processes, including tumorigenesis. This study aimed to characterize the biological mechanism of taurine-upregulated gene 1 (TUG1) in colon cancer. MATERIAL/METHODS: qRT-PCR was used to analyze the expression level of TUG1 and p63 in 75 colon cancer tissues and the matched adjacent non-tumor tissue. In vitro, cultured colon cancer cell lines HCT-116 and LoVo were used as cell models. TUG1 and p63 were silenced via transferring siRNA into HCT-116 or LoVo. The effects of TUG1 were investigated by examining cell proliferation, apoptosis, and migration. RESULTS: Among the 75 colon cancer cases, the expression of TUG1 was significantly higher in colon cancer tissues compared with the matched adjacent non-tumor tissue, while p63 expression was lower in the tumor tissue. In HCT-116 and LoVo, the expression of TUG1 was significantly increased by p63 siRNA transfection. Furthermore, down-regulation of TUG1 by siRNA significantly inhibited the cell proliferation and promoted colon cancer cell apoptosis. In addition, inhibition of TUG1 expression significantly blocked the cell migration ability of colon cancer cells. CONCLUSIONS: LncRNA TUG1 may serve as a potential oncogene for colon cancer. Overexpressed TUG1 may contribute to promoting cell proliferation and migration in colon cancer cells. International Scientific Literature, Inc. 2016-09-16 /pmc/articles/PMC5027858/ /pubmed/27634385 http://dx.doi.org/10.12659/MSM.897072 Text en © Med Sci Monit, 2016 This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) |
spellingShingle | Molecular Biology Zhai, Hui-yuan Sui, Ming-hua Yu, Xiao Qu, Zhen Hu, Jin-chen Sun, Hai-qing Zheng, Hai-tao Zhou, Kai Jiang, Li-xin Overexpression of Long Non-Coding RNA TUG1 Promotes Colon Cancer Progression |
title | Overexpression of Long Non-Coding RNA TUG1 Promotes Colon Cancer Progression |
title_full | Overexpression of Long Non-Coding RNA TUG1 Promotes Colon Cancer Progression |
title_fullStr | Overexpression of Long Non-Coding RNA TUG1 Promotes Colon Cancer Progression |
title_full_unstemmed | Overexpression of Long Non-Coding RNA TUG1 Promotes Colon Cancer Progression |
title_short | Overexpression of Long Non-Coding RNA TUG1 Promotes Colon Cancer Progression |
title_sort | overexpression of long non-coding rna tug1 promotes colon cancer progression |
topic | Molecular Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5027858/ https://www.ncbi.nlm.nih.gov/pubmed/27634385 http://dx.doi.org/10.12659/MSM.897072 |
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