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Overexpression of Contactin 1 promotes growth, migration and invasion in Hs578T breast cancer cells
BACKGROUND: Contactin1 (CNTN1) has been shown to play an important role in the invasion and metastasis of several tumors; however, the role of CNTN1 in breast cancer has not been fully studied. The purpose of this study is to investigate the role of CNTN1 in regulating tumor growth, migration and in...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5907708/ https://www.ncbi.nlm.nih.gov/pubmed/29673312 http://dx.doi.org/10.1186/s12860-018-0154-3 |
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author | Chen, Nan He, Sai Geng, Jie Song, Zhang-Jun Han, Pi-Hua Qin, Juan Zhao, Zheng Song, Yong-Chun Wang, Hu-Xia Dang, Cheng-Xue |
author_facet | Chen, Nan He, Sai Geng, Jie Song, Zhang-Jun Han, Pi-Hua Qin, Juan Zhao, Zheng Song, Yong-Chun Wang, Hu-Xia Dang, Cheng-Xue |
author_sort | Chen, Nan |
collection | PubMed |
description | BACKGROUND: Contactin1 (CNTN1) has been shown to play an important role in the invasion and metastasis of several tumors; however, the role of CNTN1 in breast cancer has not been fully studied. The purpose of this study is to investigate the role of CNTN1 in regulating tumor growth, migration and invasion in breast cancer. RESULTS: To investigate its function, CNTN1 was expressed in Hs578T cells. CNTN1 expression was confirmed by western blot, immunohistochemistry and real-time RT-PCR. The effect of CNTN1 overexpression on proliferation, migration and invasion of Hs578T breast cancer cells was assessed in vitro and in vivo. Our results showed that CNTN1 overexpression promoted Hs578T cell proliferation, cell cycle progression, colony formation, invasion and migration. Notably, overexpression of CNTN1 in Hs578T cells enhanced the growth of mouse xenograft tumors. CONCLUSIONS: CNTN1 promotes growth, metastasis and invasion of Hs578T breast cancer cell line. Thus, therapies targeting CNTN1 may prove efficacious for breast cancer. However, further investigation is required to understand the mechanism by which CNTN1 influences proliferation, metastasis and invasion in breast cancer. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12860-018-0154-3) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-5907708 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-59077082018-04-30 Overexpression of Contactin 1 promotes growth, migration and invasion in Hs578T breast cancer cells Chen, Nan He, Sai Geng, Jie Song, Zhang-Jun Han, Pi-Hua Qin, Juan Zhao, Zheng Song, Yong-Chun Wang, Hu-Xia Dang, Cheng-Xue BMC Cell Biol Research Article BACKGROUND: Contactin1 (CNTN1) has been shown to play an important role in the invasion and metastasis of several tumors; however, the role of CNTN1 in breast cancer has not been fully studied. The purpose of this study is to investigate the role of CNTN1 in regulating tumor growth, migration and invasion in breast cancer. RESULTS: To investigate its function, CNTN1 was expressed in Hs578T cells. CNTN1 expression was confirmed by western blot, immunohistochemistry and real-time RT-PCR. The effect of CNTN1 overexpression on proliferation, migration and invasion of Hs578T breast cancer cells was assessed in vitro and in vivo. Our results showed that CNTN1 overexpression promoted Hs578T cell proliferation, cell cycle progression, colony formation, invasion and migration. Notably, overexpression of CNTN1 in Hs578T cells enhanced the growth of mouse xenograft tumors. CONCLUSIONS: CNTN1 promotes growth, metastasis and invasion of Hs578T breast cancer cell line. Thus, therapies targeting CNTN1 may prove efficacious for breast cancer. However, further investigation is required to understand the mechanism by which CNTN1 influences proliferation, metastasis and invasion in breast cancer. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12860-018-0154-3) contains supplementary material, which is available to authorized users. BioMed Central 2018-04-19 /pmc/articles/PMC5907708/ /pubmed/29673312 http://dx.doi.org/10.1186/s12860-018-0154-3 Text en © The Author(s). 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Chen, Nan He, Sai Geng, Jie Song, Zhang-Jun Han, Pi-Hua Qin, Juan Zhao, Zheng Song, Yong-Chun Wang, Hu-Xia Dang, Cheng-Xue Overexpression of Contactin 1 promotes growth, migration and invasion in Hs578T breast cancer cells |
title | Overexpression of Contactin 1 promotes growth, migration and invasion in Hs578T breast cancer cells |
title_full | Overexpression of Contactin 1 promotes growth, migration and invasion in Hs578T breast cancer cells |
title_fullStr | Overexpression of Contactin 1 promotes growth, migration and invasion in Hs578T breast cancer cells |
title_full_unstemmed | Overexpression of Contactin 1 promotes growth, migration and invasion in Hs578T breast cancer cells |
title_short | Overexpression of Contactin 1 promotes growth, migration and invasion in Hs578T breast cancer cells |
title_sort | overexpression of contactin 1 promotes growth, migration and invasion in hs578t breast cancer cells |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5907708/ https://www.ncbi.nlm.nih.gov/pubmed/29673312 http://dx.doi.org/10.1186/s12860-018-0154-3 |
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