USP25 Regulates the Proliferation and Apoptosis of Ovarian Granulosa Cells in Polycystic Ovary Syndrome by Modulating the PI3K/AKT Pathway via Deubiquitinating PTEN

Background: Polycystic ovarian syndrome (PCOS) is an endocrine-related disease related to abnormal folliculogenesis and is a leading cause of infertility worldwide. Inhibition of granulosa cells (GCs) proliferation and increased GCs apoptosis have been identified as the major factors in aberrant fol...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Yue Gao, Jiao Chen, Rui Ji, Jinli Ding, Yan Zhang, Jing Yang
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	USP25 PTEN PCOS PI3K/AKT deubiquitinating Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/9b2543bf2ced48c5a78e0829bea7ad32
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:9b2543bf2ced48c5a78e0829bea7ad32
record_format	dspace
spelling	oai:doaj.org-article:9b2543bf2ced48c5a78e0829bea7ad322021-11-04T05:27:58ZUSP25 Regulates the Proliferation and Apoptosis of Ovarian Granulosa Cells in Polycystic Ovary Syndrome by Modulating the PI3K/AKT Pathway via Deubiquitinating PTEN2296-634X10.3389/fcell.2021.779718https://doaj.org/article/9b2543bf2ced48c5a78e0829bea7ad322021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fcell.2021.779718/fullhttps://doaj.org/toc/2296-634XBackground: Polycystic ovarian syndrome (PCOS) is an endocrine-related disease related to abnormal folliculogenesis and is a leading cause of infertility worldwide. Inhibition of granulosa cells (GCs) proliferation and increased GCs apoptosis have been identified as the major factors in aberrant follicle maturation.Methods: USP25 and PTEN expression in GCs from women with and without PCOS was analyzed using Western blotting. A PCOS-like mouse model was constructed using USP25 knockout and wild-type mice to explore the role of USP25 in PCOS. The human granular cell line KGN was cultured for proliferation and apoptosis assays, and the effect of USP25 on PTEN was investigated after transfection with shRNA-USP25 lentivirus.Results: USP25 expression was found to be elevated in patients and mice with PCOS. With mouse model, we observed a reduction in PCOS symptoms in mice after USP25 deletion. Increased proliferation, reduced apoptosis, activation of the phosphoinositide-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway and decreased PTEN expression were found in KGN cells after USP25 knockdown. Finally, we verified that USP25 could deubiquitinate PTEN in KGN cells.Conclusions: In this study, we investigated that USP25 can regulate the PI3K/AKT signaling pathway by deubiquitinating PTEN, thus affecting the proliferation and apoptosis of GCs and contributing to the pathogenesis of PCOS.Yue GaoJiao ChenRui JiJinli DingYan ZhangJing YangFrontiers Media S.A.articleUSP25PTENPCOSPI3K/AKTdeubiquitinatingBiology (General)QH301-705.5ENFrontiers in Cell and Developmental Biology, Vol 9 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	USP25 PTEN PCOS PI3K/AKT deubiquitinating Biology (General) QH301-705.5
spellingShingle	USP25 PTEN PCOS PI3K/AKT deubiquitinating Biology (General) QH301-705.5 Yue Gao Jiao Chen Rui Ji Jinli Ding Yan Zhang Jing Yang USP25 Regulates the Proliferation and Apoptosis of Ovarian Granulosa Cells in Polycystic Ovary Syndrome by Modulating the PI3K/AKT Pathway via Deubiquitinating PTEN
description	Background: Polycystic ovarian syndrome (PCOS) is an endocrine-related disease related to abnormal folliculogenesis and is a leading cause of infertility worldwide. Inhibition of granulosa cells (GCs) proliferation and increased GCs apoptosis have been identified as the major factors in aberrant follicle maturation.Methods: USP25 and PTEN expression in GCs from women with and without PCOS was analyzed using Western blotting. A PCOS-like mouse model was constructed using USP25 knockout and wild-type mice to explore the role of USP25 in PCOS. The human granular cell line KGN was cultured for proliferation and apoptosis assays, and the effect of USP25 on PTEN was investigated after transfection with shRNA-USP25 lentivirus.Results: USP25 expression was found to be elevated in patients and mice with PCOS. With mouse model, we observed a reduction in PCOS symptoms in mice after USP25 deletion. Increased proliferation, reduced apoptosis, activation of the phosphoinositide-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway and decreased PTEN expression were found in KGN cells after USP25 knockdown. Finally, we verified that USP25 could deubiquitinate PTEN in KGN cells.Conclusions: In this study, we investigated that USP25 can regulate the PI3K/AKT signaling pathway by deubiquitinating PTEN, thus affecting the proliferation and apoptosis of GCs and contributing to the pathogenesis of PCOS.
format	article
author	Yue Gao Jiao Chen Rui Ji Jinli Ding Yan Zhang Jing Yang
author_facet	Yue Gao Jiao Chen Rui Ji Jinli Ding Yan Zhang Jing Yang
author_sort	Yue Gao
title	USP25 Regulates the Proliferation and Apoptosis of Ovarian Granulosa Cells in Polycystic Ovary Syndrome by Modulating the PI3K/AKT Pathway via Deubiquitinating PTEN
title_short	USP25 Regulates the Proliferation and Apoptosis of Ovarian Granulosa Cells in Polycystic Ovary Syndrome by Modulating the PI3K/AKT Pathway via Deubiquitinating PTEN
title_full	USP25 Regulates the Proliferation and Apoptosis of Ovarian Granulosa Cells in Polycystic Ovary Syndrome by Modulating the PI3K/AKT Pathway via Deubiquitinating PTEN
title_fullStr	USP25 Regulates the Proliferation and Apoptosis of Ovarian Granulosa Cells in Polycystic Ovary Syndrome by Modulating the PI3K/AKT Pathway via Deubiquitinating PTEN
title_full_unstemmed	USP25 Regulates the Proliferation and Apoptosis of Ovarian Granulosa Cells in Polycystic Ovary Syndrome by Modulating the PI3K/AKT Pathway via Deubiquitinating PTEN
title_sort	usp25 regulates the proliferation and apoptosis of ovarian granulosa cells in polycystic ovary syndrome by modulating the pi3k/akt pathway via deubiquitinating pten
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/9b2543bf2ced48c5a78e0829bea7ad32
work_keys_str_mv	AT yuegao usp25regulatestheproliferationandapoptosisofovariangranulosacellsinpolycysticovarysyndromebymodulatingthepi3kaktpathwayviadeubiquitinatingpten AT jiaochen usp25regulatestheproliferationandapoptosisofovariangranulosacellsinpolycysticovarysyndromebymodulatingthepi3kaktpathwayviadeubiquitinatingpten AT ruiji usp25regulatestheproliferationandapoptosisofovariangranulosacellsinpolycysticovarysyndromebymodulatingthepi3kaktpathwayviadeubiquitinatingpten AT jinliding usp25regulatestheproliferationandapoptosisofovariangranulosacellsinpolycysticovarysyndromebymodulatingthepi3kaktpathwayviadeubiquitinatingpten AT yanzhang usp25regulatestheproliferationandapoptosisofovariangranulosacellsinpolycysticovarysyndromebymodulatingthepi3kaktpathwayviadeubiquitinatingpten AT jingyang usp25regulatestheproliferationandapoptosisofovariangranulosacellsinpolycysticovarysyndromebymodulatingthepi3kaktpathwayviadeubiquitinatingpten
_version_	1718445228101206016

USP25 Regulates the Proliferation and Apoptosis of Ovarian Granulosa Cells in Polycystic Ovary Syndrome by Modulating the PI3K/AKT Pathway via Deubiquitinating PTEN

Ejemplares similares