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Upregulation of FOXP4 in breast cancer promotes migration and invasion through facilitating EMT
BACKGROUND: Family of forkhead box transcription factors has been found to play key roles in multiple types of cancer. MATERIALS AND METHODS: Our study is to decipher the effects of FOXP4 in human breast cancer (BC). Quantitative real-time polymerase chain reaction and Western blot analyses were per...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6459146/ https://www.ncbi.nlm.nih.gov/pubmed/31040716 http://dx.doi.org/10.2147/CMAR.S191641 |
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author | Ma, Tao Zhang, Jin |
author_facet | Ma, Tao Zhang, Jin |
author_sort | Ma, Tao |
collection | PubMed |
description | BACKGROUND: Family of forkhead box transcription factors has been found to play key roles in multiple types of cancer. MATERIALS AND METHODS: Our study is to decipher the effects of FOXP4 in human breast cancer (BC). Quantitative real-time polymerase chain reaction and Western blot analyses were performed to determine the mRNA and protein expressions of FOXP4 in BC tissue samples and cell lines. The gain and loss of function assay were used to explore the detailed roles of FOXP4 in breast cell lines, including MDA-MB-231 and MCF-7 cells. Its effect on BC growth, migration, and invasion were evaluated by colony formation assay, CCK-8 assay, wound-healing assay, and transwell invasion assay, respectively. RESULTS: Our findings revealed that FOXP4 promotes cell proliferation, migration, as well as invasion of BC cells. Furthermore, FOXP4 also facilitates epithelial–mesenchymal transition. ChIP, qChIP assay, and dual luciferase reporter assay were used to examine whether Snail is a downstream target of FOXP4. Moreover, overexpression of Snail could partially rescue the effects of FOXP4 inhibition on cancer cell migration and invasion. CONCLUSION: Our findings revealed that FOXP4 is a critical regulator in BC. |
format | Online Article Text |
id | pubmed-6459146 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-64591462019-04-30 Upregulation of FOXP4 in breast cancer promotes migration and invasion through facilitating EMT Ma, Tao Zhang, Jin Cancer Manag Res Original Research BACKGROUND: Family of forkhead box transcription factors has been found to play key roles in multiple types of cancer. MATERIALS AND METHODS: Our study is to decipher the effects of FOXP4 in human breast cancer (BC). Quantitative real-time polymerase chain reaction and Western blot analyses were performed to determine the mRNA and protein expressions of FOXP4 in BC tissue samples and cell lines. The gain and loss of function assay were used to explore the detailed roles of FOXP4 in breast cell lines, including MDA-MB-231 and MCF-7 cells. Its effect on BC growth, migration, and invasion were evaluated by colony formation assay, CCK-8 assay, wound-healing assay, and transwell invasion assay, respectively. RESULTS: Our findings revealed that FOXP4 promotes cell proliferation, migration, as well as invasion of BC cells. Furthermore, FOXP4 also facilitates epithelial–mesenchymal transition. ChIP, qChIP assay, and dual luciferase reporter assay were used to examine whether Snail is a downstream target of FOXP4. Moreover, overexpression of Snail could partially rescue the effects of FOXP4 inhibition on cancer cell migration and invasion. CONCLUSION: Our findings revealed that FOXP4 is a critical regulator in BC. Dove Medical Press 2019-04-08 /pmc/articles/PMC6459146/ /pubmed/31040716 http://dx.doi.org/10.2147/CMAR.S191641 Text en © 2019 Ma and Zhang. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. |
spellingShingle | Original Research Ma, Tao Zhang, Jin Upregulation of FOXP4 in breast cancer promotes migration and invasion through facilitating EMT |
title | Upregulation of FOXP4 in breast cancer promotes migration and invasion through facilitating EMT |
title_full | Upregulation of FOXP4 in breast cancer promotes migration and invasion through facilitating EMT |
title_fullStr | Upregulation of FOXP4 in breast cancer promotes migration and invasion through facilitating EMT |
title_full_unstemmed | Upregulation of FOXP4 in breast cancer promotes migration and invasion through facilitating EMT |
title_short | Upregulation of FOXP4 in breast cancer promotes migration and invasion through facilitating EMT |
title_sort | upregulation of foxp4 in breast cancer promotes migration and invasion through facilitating emt |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6459146/ https://www.ncbi.nlm.nih.gov/pubmed/31040716 http://dx.doi.org/10.2147/CMAR.S191641 |
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