Fukutin Protein Participates in Cell Proliferation by Enhancing Cyclin D1 Expression through Binding to the Transcription Factor Activator Protein-1: An In Vitro Study

The causative gene of Fukuyama congenital muscular dystrophy (fukutin) is involved in formation of the basement membrane through glycosylation of alpha-dystroglycan. However, there are other proposed functions that have not been fully understood. Using cultured astrocytes (1321N1), we found nuclear...

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Autores principales:	Yukinori Okamura, Tomoko Yamamoto, Ryota Tsukui, Yoichiro Kato, Noriyuki Shibata
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	activator protein-1 astrocytes cell proliferation c-Jun cyclin D1 fukutin Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/1a29f381841b4c1394cd09f85622ff29
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spelling	oai:doaj.org-article:1a29f381841b4c1394cd09f85622ff292021-11-25T17:53:50ZFukutin Protein Participates in Cell Proliferation by Enhancing Cyclin D1 Expression through Binding to the Transcription Factor Activator Protein-1: An In Vitro Study10.3390/ijms2222121531422-00671661-6596https://doaj.org/article/1a29f381841b4c1394cd09f85622ff292021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/22/12153https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067The causative gene of Fukuyama congenital muscular dystrophy (fukutin) is involved in formation of the basement membrane through glycosylation of alpha-dystroglycan. However, there are other proposed functions that have not been fully understood. Using cultured astrocytes (1321N1), we found nuclear localization of fukutin and a positive relationship between fukutin expression and cell proliferation. Among potential proteins regulating cell proliferation, we focused on cyclin D1, by reverse-transcription polymerase chain reaction, Western blotting, immunocytochemistry, enzyme-linked immunosorbent assay (ELISA), and sandwich ELISA. Expression of cyclin D1 was significantly downregulated by fukutin knockdown and significantly upregulated by fukutin overexpression. Moreover, fukutin was proven to bind to the activator protein-1 (AP-1) binding site of cyclin D1 promoter, as well as the AP-1 component c-Jun. The c-Jun phosphorylation status was not significantly influenced by knockdown or overexpression of fukutin. The present results provide in vitro evidence for a novel function of fukutin, which participates in cell proliferation by enhancing cyclin D1 expression through forming a complex with AP-1. It is likely that fukutin is a potential cofactor of AP-1.Yukinori OkamuraTomoko YamamotoRyota TsukuiYoichiro KatoNoriyuki ShibataMDPI AGarticleactivator protein-1astrocytescell proliferationc-Juncyclin D1fukutinBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 12153, p 12153 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	activator protein-1 astrocytes cell proliferation c-Jun cyclin D1 fukutin Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	activator protein-1 astrocytes cell proliferation c-Jun cyclin D1 fukutin Biology (General) QH301-705.5 Chemistry QD1-999 Yukinori Okamura Tomoko Yamamoto Ryota Tsukui Yoichiro Kato Noriyuki Shibata Fukutin Protein Participates in Cell Proliferation by Enhancing Cyclin D1 Expression through Binding to the Transcription Factor Activator Protein-1: An In Vitro Study
description	The causative gene of Fukuyama congenital muscular dystrophy (fukutin) is involved in formation of the basement membrane through glycosylation of alpha-dystroglycan. However, there are other proposed functions that have not been fully understood. Using cultured astrocytes (1321N1), we found nuclear localization of fukutin and a positive relationship between fukutin expression and cell proliferation. Among potential proteins regulating cell proliferation, we focused on cyclin D1, by reverse-transcription polymerase chain reaction, Western blotting, immunocytochemistry, enzyme-linked immunosorbent assay (ELISA), and sandwich ELISA. Expression of cyclin D1 was significantly downregulated by fukutin knockdown and significantly upregulated by fukutin overexpression. Moreover, fukutin was proven to bind to the activator protein-1 (AP-1) binding site of cyclin D1 promoter, as well as the AP-1 component c-Jun. The c-Jun phosphorylation status was not significantly influenced by knockdown or overexpression of fukutin. The present results provide in vitro evidence for a novel function of fukutin, which participates in cell proliferation by enhancing cyclin D1 expression through forming a complex with AP-1. It is likely that fukutin is a potential cofactor of AP-1.
format	article
author	Yukinori Okamura Tomoko Yamamoto Ryota Tsukui Yoichiro Kato Noriyuki Shibata
author_facet	Yukinori Okamura Tomoko Yamamoto Ryota Tsukui Yoichiro Kato Noriyuki Shibata
author_sort	Yukinori Okamura
title	Fukutin Protein Participates in Cell Proliferation by Enhancing Cyclin D1 Expression through Binding to the Transcription Factor Activator Protein-1: An In Vitro Study
title_short	Fukutin Protein Participates in Cell Proliferation by Enhancing Cyclin D1 Expression through Binding to the Transcription Factor Activator Protein-1: An In Vitro Study
title_full	Fukutin Protein Participates in Cell Proliferation by Enhancing Cyclin D1 Expression through Binding to the Transcription Factor Activator Protein-1: An In Vitro Study
title_fullStr	Fukutin Protein Participates in Cell Proliferation by Enhancing Cyclin D1 Expression through Binding to the Transcription Factor Activator Protein-1: An In Vitro Study
title_full_unstemmed	Fukutin Protein Participates in Cell Proliferation by Enhancing Cyclin D1 Expression through Binding to the Transcription Factor Activator Protein-1: An In Vitro Study
title_sort	fukutin protein participates in cell proliferation by enhancing cyclin d1 expression through binding to the transcription factor activator protein-1: an in vitro study
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/1a29f381841b4c1394cd09f85622ff29
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Fukutin Protein Participates in Cell Proliferation by Enhancing Cyclin D1 Expression through Binding to the Transcription Factor Activator Protein-1: An In Vitro Study

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