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Up-regulation of S100A16 expression promotes epithelial-mesenchymal transition via Notch1 pathway in breast cancer
BACKGROUND: Our previous studies demonstrated that S100A16 promotes adipogenesis and is involved in weight gain attenuation induced by dietary calcium. Till now, the function of S100A16 in the breast cancer remains to be elucidated. RESULTS: In this study, we observed that S100A16 was expressed in h...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4197258/ https://www.ncbi.nlm.nih.gov/pubmed/25287362 http://dx.doi.org/10.1186/s12929-014-0097-8 |
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author | Zhou, Wenbin Pan, Hong Xia, Tiansong Xue, Jinqiu Cheng, Lin Fan, Ping Zhang, Yifen Zhu, Weidong Xue, Yi Liu, Xiaoan Ding, Qiang Liu, Yun Wang, Shui |
author_facet | Zhou, Wenbin Pan, Hong Xia, Tiansong Xue, Jinqiu Cheng, Lin Fan, Ping Zhang, Yifen Zhu, Weidong Xue, Yi Liu, Xiaoan Ding, Qiang Liu, Yun Wang, Shui |
author_sort | Zhou, Wenbin |
collection | PubMed |
description | BACKGROUND: Our previous studies demonstrated that S100A16 promotes adipogenesis and is involved in weight gain attenuation induced by dietary calcium. Till now, the function of S100A16 in the breast cancer remains to be elucidated. RESULTS: In this study, we observed that S100A16 was expressed in higher levels in human breast cancer tissues compared with paired adjacent non-cancerous tissues. Further examination showed that overexpression of S100A16 in MCF-7 cells could increase cell proliferation and colony formation. One major mechanistic change was that S100A16 was able to up-regulate the transcription factors Notch1, ZEB1, and ZEB2, which had the capacities to directly repress the expression of epithelial markers E-cadherin and β-catenin but increase mesenchymal markers N-cadherin and vimentin, a characterized phenotype of epithelial-mensenchymal transition (EMT). In addition to display with morphologic change, migration and invasion were increased in S100A16 over-expressed MCF-7 cells. Importantly, knockdown of Notch1 by specific siRNA could reverse the EMT induced by S100A16 overexpression, which confirmed that Notch1 played a critical role in the process of EMT induced by S100A16. CONCLUSIONS: All together, our data indicated that S100A16 had a potential function to regulate some embryonic transcription factors to promote EMT in breast cancer cells which may be an important target site for the therapy of breast cancer. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12929-014-0097-8) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-4197258 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-41972582014-10-16 Up-regulation of S100A16 expression promotes epithelial-mesenchymal transition via Notch1 pathway in breast cancer Zhou, Wenbin Pan, Hong Xia, Tiansong Xue, Jinqiu Cheng, Lin Fan, Ping Zhang, Yifen Zhu, Weidong Xue, Yi Liu, Xiaoan Ding, Qiang Liu, Yun Wang, Shui J Biomed Sci Research BACKGROUND: Our previous studies demonstrated that S100A16 promotes adipogenesis and is involved in weight gain attenuation induced by dietary calcium. Till now, the function of S100A16 in the breast cancer remains to be elucidated. RESULTS: In this study, we observed that S100A16 was expressed in higher levels in human breast cancer tissues compared with paired adjacent non-cancerous tissues. Further examination showed that overexpression of S100A16 in MCF-7 cells could increase cell proliferation and colony formation. One major mechanistic change was that S100A16 was able to up-regulate the transcription factors Notch1, ZEB1, and ZEB2, which had the capacities to directly repress the expression of epithelial markers E-cadherin and β-catenin but increase mesenchymal markers N-cadherin and vimentin, a characterized phenotype of epithelial-mensenchymal transition (EMT). In addition to display with morphologic change, migration and invasion were increased in S100A16 over-expressed MCF-7 cells. Importantly, knockdown of Notch1 by specific siRNA could reverse the EMT induced by S100A16 overexpression, which confirmed that Notch1 played a critical role in the process of EMT induced by S100A16. CONCLUSIONS: All together, our data indicated that S100A16 had a potential function to regulate some embryonic transcription factors to promote EMT in breast cancer cells which may be an important target site for the therapy of breast cancer. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12929-014-0097-8) contains supplementary material, which is available to authorized users. BioMed Central 2014-10-07 /pmc/articles/PMC4197258/ /pubmed/25287362 http://dx.doi.org/10.1186/s12929-014-0097-8 Text en © Zhou et al.; licensee BioMed Central Ltd. 2014 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. 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 Zhou, Wenbin Pan, Hong Xia, Tiansong Xue, Jinqiu Cheng, Lin Fan, Ping Zhang, Yifen Zhu, Weidong Xue, Yi Liu, Xiaoan Ding, Qiang Liu, Yun Wang, Shui Up-regulation of S100A16 expression promotes epithelial-mesenchymal transition via Notch1 pathway in breast cancer |
title | Up-regulation of S100A16 expression promotes epithelial-mesenchymal transition via Notch1 pathway in breast cancer |
title_full | Up-regulation of S100A16 expression promotes epithelial-mesenchymal transition via Notch1 pathway in breast cancer |
title_fullStr | Up-regulation of S100A16 expression promotes epithelial-mesenchymal transition via Notch1 pathway in breast cancer |
title_full_unstemmed | Up-regulation of S100A16 expression promotes epithelial-mesenchymal transition via Notch1 pathway in breast cancer |
title_short | Up-regulation of S100A16 expression promotes epithelial-mesenchymal transition via Notch1 pathway in breast cancer |
title_sort | up-regulation of s100a16 expression promotes epithelial-mesenchymal transition via notch1 pathway in breast cancer |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4197258/ https://www.ncbi.nlm.nih.gov/pubmed/25287362 http://dx.doi.org/10.1186/s12929-014-0097-8 |
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