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FAD104, a regulator of adipogenesis, is a novel suppressor of TGF-β–mediated EMT in cervical cancer cells
Epithelial-to-mesenchymal transition (EMT) is a biological process in which epithelial cells translate into a mesenchymal phenotype with invasive capacities, contributing to tumour progression, metastasis, and the acquisition of chemotherapy resistance. To identify new therapeutic targets for cancer...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5703855/ https://www.ncbi.nlm.nih.gov/pubmed/29180690 http://dx.doi.org/10.1038/s41598-017-16555-3 |
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author | Goto, Motoharu Osada, Shigehiro Imagawa, Masayoshi Nishizuka, Makoto |
author_facet | Goto, Motoharu Osada, Shigehiro Imagawa, Masayoshi Nishizuka, Makoto |
author_sort | Goto, Motoharu |
collection | PubMed |
description | Epithelial-to-mesenchymal transition (EMT) is a biological process in which epithelial cells translate into a mesenchymal phenotype with invasive capacities, contributing to tumour progression, metastasis, and the acquisition of chemotherapy resistance. To identify new therapeutic targets for cancers, it is important to clarify the molecular mechanism of induction of EMT. We have previously reported that fad104, a positive regulator of adipocyte differentiation, suppressed the invasion and metastasis of melanoma and breast cancer cells. In this study, we showed that FAD104 functions as a novel suppressor of transforming growth factor-β (TGF-β)–mediated EMT in cervical cancer cells. Expression of FAD104 is upregulated during TGF-β–mediated EMT in human cervical cancer HeLa cells. Reduction of fad104 expression enhanced TGF-β–mediated EMT and migration in HeLa cells. Conversely, overexpression of FAD104 suppressed TGF-β–induced EMT. In addition, we showed that FAD104 negatively regulated phosphorylation of Smad2 and Smad3 but positively regulated phosphorylation of Smad1/5/8 via treatment with TGF-β. These findings demonstrate that FAD104 is a novel suppressor of TGF-β signalling and represses TGF-β–mediated EMT in cervical cancer cells. |
format | Online Article Text |
id | pubmed-5703855 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-57038552017-11-30 FAD104, a regulator of adipogenesis, is a novel suppressor of TGF-β–mediated EMT in cervical cancer cells Goto, Motoharu Osada, Shigehiro Imagawa, Masayoshi Nishizuka, Makoto Sci Rep Article Epithelial-to-mesenchymal transition (EMT) is a biological process in which epithelial cells translate into a mesenchymal phenotype with invasive capacities, contributing to tumour progression, metastasis, and the acquisition of chemotherapy resistance. To identify new therapeutic targets for cancers, it is important to clarify the molecular mechanism of induction of EMT. We have previously reported that fad104, a positive regulator of adipocyte differentiation, suppressed the invasion and metastasis of melanoma and breast cancer cells. In this study, we showed that FAD104 functions as a novel suppressor of transforming growth factor-β (TGF-β)–mediated EMT in cervical cancer cells. Expression of FAD104 is upregulated during TGF-β–mediated EMT in human cervical cancer HeLa cells. Reduction of fad104 expression enhanced TGF-β–mediated EMT and migration in HeLa cells. Conversely, overexpression of FAD104 suppressed TGF-β–induced EMT. In addition, we showed that FAD104 negatively regulated phosphorylation of Smad2 and Smad3 but positively regulated phosphorylation of Smad1/5/8 via treatment with TGF-β. These findings demonstrate that FAD104 is a novel suppressor of TGF-β signalling and represses TGF-β–mediated EMT in cervical cancer cells. Nature Publishing Group UK 2017-11-27 /pmc/articles/PMC5703855/ /pubmed/29180690 http://dx.doi.org/10.1038/s41598-017-16555-3 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Goto, Motoharu Osada, Shigehiro Imagawa, Masayoshi Nishizuka, Makoto FAD104, a regulator of adipogenesis, is a novel suppressor of TGF-β–mediated EMT in cervical cancer cells |
title | FAD104, a regulator of adipogenesis, is a novel suppressor of TGF-β–mediated EMT in cervical cancer cells |
title_full | FAD104, a regulator of adipogenesis, is a novel suppressor of TGF-β–mediated EMT in cervical cancer cells |
title_fullStr | FAD104, a regulator of adipogenesis, is a novel suppressor of TGF-β–mediated EMT in cervical cancer cells |
title_full_unstemmed | FAD104, a regulator of adipogenesis, is a novel suppressor of TGF-β–mediated EMT in cervical cancer cells |
title_short | FAD104, a regulator of adipogenesis, is a novel suppressor of TGF-β–mediated EMT in cervical cancer cells |
title_sort | fad104, a regulator of adipogenesis, is a novel suppressor of tgf-β–mediated emt in cervical cancer cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5703855/ https://www.ncbi.nlm.nih.gov/pubmed/29180690 http://dx.doi.org/10.1038/s41598-017-16555-3 |
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