Lysosomal activity maintains glycolysis and cyclin E1 expression by mediating Ad4BP/SF-1 stability for proper steroidogenic cell growth

Abstract The development and differentiation of steroidogenic organs are controlled by Ad4BP/SF-1 (adrenal 4 binding protein/steroidogenic factor 1). Besides, lysosomal activity is required for steroidogenesis and also enables adrenocortical cell to survive during stress. However, the role of lysoso...

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Autores principales:	Jhih-Siang Syu, Takashi Baba, Jyun-Yuan Huang, Hidesato Ogawa, Chi-Han Hsieh, Jin-Xian Hu, Ting-Yu Chen, Tzu-Chien Lin, Megumi Tsuchiya, Ken-Ichirou Morohashi, Bu-Miin Huang, Fu-l. Lu, Chia-Yih Wang
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/35ade0a21f8d4166b02d00fb684be8c8
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spelling	oai:doaj.org-article:35ade0a21f8d4166b02d00fb684be8c82021-12-02T11:53:02ZLysosomal activity maintains glycolysis and cyclin E1 expression by mediating Ad4BP/SF-1 stability for proper steroidogenic cell growth10.1038/s41598-017-00393-42045-2322https://doaj.org/article/35ade0a21f8d4166b02d00fb684be8c82017-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-00393-4https://doaj.org/toc/2045-2322Abstract The development and differentiation of steroidogenic organs are controlled by Ad4BP/SF-1 (adrenal 4 binding protein/steroidogenic factor 1). Besides, lysosomal activity is required for steroidogenesis and also enables adrenocortical cell to survive during stress. However, the role of lysosomal activity on steroidogenic cell growth is as yet unknown. Here, we showed that lysosomal activity maintained Ad4BP/SF-1 protein stability for proper steroidogenic cell growth. Treatment of cells with lysosomal inhibitors reduced steroidogenic cell growth in vitro. Suppression of autophagy did not affect cell growth indicating that autophagy was dispensable for steroidogenic cell growth. When lysosomal activity was inhibited, the protein stability of Ad4BP/SF-1 was reduced leading to reduced S phase entry. Interestingly, treatment of cells with lysosomal inhibitors reduced glycolytic gene expression and supplying the cells with pyruvate alleviated the growth defect. ChIP-sequence/ChIP studies indicated that Ad4BP/SF-1 binds to the upstream region of Ccne1 (cyclin E1) gene during G1/S phase. In addition, treatment of zebrafish embryo with lysosomal inhibitor reduced the levels of the interrenal (adrenal) gland markers. Thus lysosomal activity maintains steroidogenic cell growth via stabilizing Ad4BP/SF-1 protein.Jhih-Siang SyuTakashi BabaJyun-Yuan HuangHidesato OgawaChi-Han HsiehJin-Xian HuTing-Yu ChenTzu-Chien LinMegumi TsuchiyaKen-Ichirou MorohashiBu-Miin HuangFu-l. LuChia-Yih WangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-14 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Jhih-Siang Syu Takashi Baba Jyun-Yuan Huang Hidesato Ogawa Chi-Han Hsieh Jin-Xian Hu Ting-Yu Chen Tzu-Chien Lin Megumi Tsuchiya Ken-Ichirou Morohashi Bu-Miin Huang Fu-l. Lu Chia-Yih Wang Lysosomal activity maintains glycolysis and cyclin E1 expression by mediating Ad4BP/SF-1 stability for proper steroidogenic cell growth
description	Abstract The development and differentiation of steroidogenic organs are controlled by Ad4BP/SF-1 (adrenal 4 binding protein/steroidogenic factor 1). Besides, lysosomal activity is required for steroidogenesis and also enables adrenocortical cell to survive during stress. However, the role of lysosomal activity on steroidogenic cell growth is as yet unknown. Here, we showed that lysosomal activity maintained Ad4BP/SF-1 protein stability for proper steroidogenic cell growth. Treatment of cells with lysosomal inhibitors reduced steroidogenic cell growth in vitro. Suppression of autophagy did not affect cell growth indicating that autophagy was dispensable for steroidogenic cell growth. When lysosomal activity was inhibited, the protein stability of Ad4BP/SF-1 was reduced leading to reduced S phase entry. Interestingly, treatment of cells with lysosomal inhibitors reduced glycolytic gene expression and supplying the cells with pyruvate alleviated the growth defect. ChIP-sequence/ChIP studies indicated that Ad4BP/SF-1 binds to the upstream region of Ccne1 (cyclin E1) gene during G1/S phase. In addition, treatment of zebrafish embryo with lysosomal inhibitor reduced the levels of the interrenal (adrenal) gland markers. Thus lysosomal activity maintains steroidogenic cell growth via stabilizing Ad4BP/SF-1 protein.
format	article
author	Jhih-Siang Syu Takashi Baba Jyun-Yuan Huang Hidesato Ogawa Chi-Han Hsieh Jin-Xian Hu Ting-Yu Chen Tzu-Chien Lin Megumi Tsuchiya Ken-Ichirou Morohashi Bu-Miin Huang Fu-l. Lu Chia-Yih Wang
author_facet	Jhih-Siang Syu Takashi Baba Jyun-Yuan Huang Hidesato Ogawa Chi-Han Hsieh Jin-Xian Hu Ting-Yu Chen Tzu-Chien Lin Megumi Tsuchiya Ken-Ichirou Morohashi Bu-Miin Huang Fu-l. Lu Chia-Yih Wang
author_sort	Jhih-Siang Syu
title	Lysosomal activity maintains glycolysis and cyclin E1 expression by mediating Ad4BP/SF-1 stability for proper steroidogenic cell growth
title_short	Lysosomal activity maintains glycolysis and cyclin E1 expression by mediating Ad4BP/SF-1 stability for proper steroidogenic cell growth
title_full	Lysosomal activity maintains glycolysis and cyclin E1 expression by mediating Ad4BP/SF-1 stability for proper steroidogenic cell growth
title_fullStr	Lysosomal activity maintains glycolysis and cyclin E1 expression by mediating Ad4BP/SF-1 stability for proper steroidogenic cell growth
title_full_unstemmed	Lysosomal activity maintains glycolysis and cyclin E1 expression by mediating Ad4BP/SF-1 stability for proper steroidogenic cell growth
title_sort	lysosomal activity maintains glycolysis and cyclin e1 expression by mediating ad4bp/sf-1 stability for proper steroidogenic cell growth
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/35ade0a21f8d4166b02d00fb684be8c8
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Lysosomal activity maintains glycolysis and cyclin E1 expression by mediating Ad4BP/SF-1 stability for proper steroidogenic cell growth

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