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CtBP1 interacts with SOX2 to promote the growth, migration and invasion of lung adenocarcinoma
Carboxyl-terminal binding protein 1 (CtBP1) is overexpressed in many types of solid tumors and has been found to be functionally associated with proliferation, migration, invasion and drug resistance of cancer cells. However, its expression pattern and functions in lung adenocarcinoma remain unclear...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6549098/ https://www.ncbi.nlm.nih.gov/pubmed/31059077 http://dx.doi.org/10.3892/or.2019.7142 |
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author | Liu, Yifei Bian, Tingting Feng, Jia Qian, Li Li, Xiaoli Zhang, Qing Zhang, Jianguo Jiang, Daishan Liu, Jian Shi, Jiahai |
author_facet | Liu, Yifei Bian, Tingting Feng, Jia Qian, Li Li, Xiaoli Zhang, Qing Zhang, Jianguo Jiang, Daishan Liu, Jian Shi, Jiahai |
author_sort | Liu, Yifei |
collection | PubMed |
description | Carboxyl-terminal binding protein 1 (CtBP1) is overexpressed in many types of solid tumors and has been found to be functionally associated with proliferation, migration, invasion and drug resistance of cancer cells. However, its expression pattern and functions in lung adenocarcinoma remain unclear. In the present study, we observed that the expression of CtBP1 was upregulated in the lung adenocarcinoma tissues of patients with lymph node metastasis and that its overexpression was correlated with tumor differentiation, size and poor overall survival. Silencing of CtBP1 by transfection with shRNA inhibited the proliferation, migration and invasion of A459 lung adenocarcinoma cells in vitro as determined by MTT assay and Transwell assay, respectively. In vivo studies using a lung patient-derived tumor xenograft (PDTX) mouse model implicated CtBP1 expression in lung adenocarcinoma growth, and further in vitro co-immunoprecipitation and depletion experiments indicated that CtBP1 regulated the biological behavior of lung adenocarcinoma cells by interacting with SOX2. Patients with elevated expression of both CtBP1 and SOX2 expression had a significantly shorter overall survival rate than patients with reduced expression of these transcripts, or than patients with elevated expression of only one transcript (P<0.01 in both cases). Taken together, these findings suggest that CtBP1 plays an important role in lung adenocarcinoma and, along with SOX2, may serve as a viable prognostic marker and therapeutic target for lung adenocarcinoma. |
format | Online Article Text |
id | pubmed-6549098 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-65490982019-06-10 CtBP1 interacts with SOX2 to promote the growth, migration and invasion of lung adenocarcinoma Liu, Yifei Bian, Tingting Feng, Jia Qian, Li Li, Xiaoli Zhang, Qing Zhang, Jianguo Jiang, Daishan Liu, Jian Shi, Jiahai Oncol Rep Articles Carboxyl-terminal binding protein 1 (CtBP1) is overexpressed in many types of solid tumors and has been found to be functionally associated with proliferation, migration, invasion and drug resistance of cancer cells. However, its expression pattern and functions in lung adenocarcinoma remain unclear. In the present study, we observed that the expression of CtBP1 was upregulated in the lung adenocarcinoma tissues of patients with lymph node metastasis and that its overexpression was correlated with tumor differentiation, size and poor overall survival. Silencing of CtBP1 by transfection with shRNA inhibited the proliferation, migration and invasion of A459 lung adenocarcinoma cells in vitro as determined by MTT assay and Transwell assay, respectively. In vivo studies using a lung patient-derived tumor xenograft (PDTX) mouse model implicated CtBP1 expression in lung adenocarcinoma growth, and further in vitro co-immunoprecipitation and depletion experiments indicated that CtBP1 regulated the biological behavior of lung adenocarcinoma cells by interacting with SOX2. Patients with elevated expression of both CtBP1 and SOX2 expression had a significantly shorter overall survival rate than patients with reduced expression of these transcripts, or than patients with elevated expression of only one transcript (P<0.01 in both cases). Taken together, these findings suggest that CtBP1 plays an important role in lung adenocarcinoma and, along with SOX2, may serve as a viable prognostic marker and therapeutic target for lung adenocarcinoma. D.A. Spandidos 2019-07 2019-05-02 /pmc/articles/PMC6549098/ /pubmed/31059077 http://dx.doi.org/10.3892/or.2019.7142 Text en Copyright: © Liu 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 Liu, Yifei Bian, Tingting Feng, Jia Qian, Li Li, Xiaoli Zhang, Qing Zhang, Jianguo Jiang, Daishan Liu, Jian Shi, Jiahai CtBP1 interacts with SOX2 to promote the growth, migration and invasion of lung adenocarcinoma |
title | CtBP1 interacts with SOX2 to promote the growth, migration and invasion of lung adenocarcinoma |
title_full | CtBP1 interacts with SOX2 to promote the growth, migration and invasion of lung adenocarcinoma |
title_fullStr | CtBP1 interacts with SOX2 to promote the growth, migration and invasion of lung adenocarcinoma |
title_full_unstemmed | CtBP1 interacts with SOX2 to promote the growth, migration and invasion of lung adenocarcinoma |
title_short | CtBP1 interacts with SOX2 to promote the growth, migration and invasion of lung adenocarcinoma |
title_sort | ctbp1 interacts with sox2 to promote the growth, migration and invasion of lung adenocarcinoma |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6549098/ https://www.ncbi.nlm.nih.gov/pubmed/31059077 http://dx.doi.org/10.3892/or.2019.7142 |
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