Transcription factor c-fos induces the development of premature ovarian insufficiency by regulating MALAT1/miR-22-3p/STAT1 network

Abstract Background The current study attempted to investigate the role of transcription factor c-fos in the development of premature ovarian insufficiency (POI) as well as the underlying mechanism involving the MALAT1/miR-22-3p/STAT1 ceRNA network. Methods Bioinformatics analysis was performed to e...

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Main Authors: Ting Qiu, Jie Zhou, Bing Ji, Liuyang Yuan, Tingsong Weng, Huishu Liu
Format: Article
Language:English
Published: BMC 2023-07-01
Series:Journal of Ovarian Research
Subjects:
Online Access:https://doi.org/10.1186/s13048-023-01212-3
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author Ting Qiu
Jie Zhou
Bing Ji
Liuyang Yuan
Tingsong Weng
Huishu Liu
author_facet Ting Qiu
Jie Zhou
Bing Ji
Liuyang Yuan
Tingsong Weng
Huishu Liu
author_sort Ting Qiu
collection DOAJ
description Abstract Background The current study attempted to investigate the role of transcription factor c-fos in the development of premature ovarian insufficiency (POI) as well as the underlying mechanism involving the MALAT1/miR-22-3p/STAT1 ceRNA network. Methods Bioinformatics analysis was performed to extract POI-related microarray dataset for identifying the target genes. Interaction among c-fos, MALAT1, miR-22-3p, and STAT1 was analyzed. An in vivo POI mouse model was prepared followed by injection of sh-c-fos and sh-STAT1 lentiviruses. Besides, an in vitro POI cell model was constructed to study the regulatory roles of c-fos, MALAT1, miR-22-3p, and STAT1. Results c-fos, MALAT1, and STAT1 were highly expressed in ovarian tissues from POI mice and CTX-induced KGN cells, while miR-22-3p was poorly expressed. c-fos targeted MALAT1 and promoted MALAT1 transcription. MALAT1 competitively bound to miR-22-3p and miR-22-3p could suppress STAT1 expression. Mechanically, c-fos aggravated ovarian function impairment in POI mice and inhibited KGN cell proliferation through regulation of the MALAT1/miR-22-3p/STAT1 regulatory network. Conclusion Our findings highlighted inducing role of the transcription factor c-fos in POI through modulation of the MALAT1/miR-22-3p/STAT1 ceRNA network.
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spelling doaj.art-94583b7b90444c9083873e13ebaf54c42023-07-23T11:22:28ZengBMCJournal of Ovarian Research1757-22152023-07-0116111410.1186/s13048-023-01212-3Transcription factor c-fos induces the development of premature ovarian insufficiency by regulating MALAT1/miR-22-3p/STAT1 networkTing Qiu0Jie Zhou1Bing Ji2Liuyang Yuan3Tingsong Weng4Huishu Liu5Department of Obstetrics and Gynecology, The First Affiliated Hospital of Jinan UniversityDepartment of Obstetrics and Gynecology, Guangzhou Women and Children’s Medical CenterDepartment of Obstetrics and Gynecology, Guangzhou Women and Children’s Medical CenterDepartment of Obstetrics and Gynecology, Guangzhou Women and Children’s Medical CenterDepartment of Obstetrics and Gynecology, Guangzhou Women and Children’s Medical CenterDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Jinan UniversityAbstract Background The current study attempted to investigate the role of transcription factor c-fos in the development of premature ovarian insufficiency (POI) as well as the underlying mechanism involving the MALAT1/miR-22-3p/STAT1 ceRNA network. Methods Bioinformatics analysis was performed to extract POI-related microarray dataset for identifying the target genes. Interaction among c-fos, MALAT1, miR-22-3p, and STAT1 was analyzed. An in vivo POI mouse model was prepared followed by injection of sh-c-fos and sh-STAT1 lentiviruses. Besides, an in vitro POI cell model was constructed to study the regulatory roles of c-fos, MALAT1, miR-22-3p, and STAT1. Results c-fos, MALAT1, and STAT1 were highly expressed in ovarian tissues from POI mice and CTX-induced KGN cells, while miR-22-3p was poorly expressed. c-fos targeted MALAT1 and promoted MALAT1 transcription. MALAT1 competitively bound to miR-22-3p and miR-22-3p could suppress STAT1 expression. Mechanically, c-fos aggravated ovarian function impairment in POI mice and inhibited KGN cell proliferation through regulation of the MALAT1/miR-22-3p/STAT1 regulatory network. Conclusion Our findings highlighted inducing role of the transcription factor c-fos in POI through modulation of the MALAT1/miR-22-3p/STAT1 ceRNA network.https://doi.org/10.1186/s13048-023-01212-3Premature ovarian insufficiency; ceRNA network; c-fos; MALAT1; miR-22-3p; STAT1
spellingShingle Ting Qiu
Jie Zhou
Bing Ji
Liuyang Yuan
Tingsong Weng
Huishu Liu
Transcription factor c-fos induces the development of premature ovarian insufficiency by regulating MALAT1/miR-22-3p/STAT1 network
Journal of Ovarian Research
Premature ovarian insufficiency; ceRNA network; c-fos; MALAT1; miR-22-3p; STAT1
title Transcription factor c-fos induces the development of premature ovarian insufficiency by regulating MALAT1/miR-22-3p/STAT1 network
title_full Transcription factor c-fos induces the development of premature ovarian insufficiency by regulating MALAT1/miR-22-3p/STAT1 network
title_fullStr Transcription factor c-fos induces the development of premature ovarian insufficiency by regulating MALAT1/miR-22-3p/STAT1 network
title_full_unstemmed Transcription factor c-fos induces the development of premature ovarian insufficiency by regulating MALAT1/miR-22-3p/STAT1 network
title_short Transcription factor c-fos induces the development of premature ovarian insufficiency by regulating MALAT1/miR-22-3p/STAT1 network
title_sort transcription factor c fos induces the development of premature ovarian insufficiency by regulating malat1 mir 22 3p stat1 network
topic Premature ovarian insufficiency; ceRNA network; c-fos; MALAT1; miR-22-3p; STAT1
url https://doi.org/10.1186/s13048-023-01212-3
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