SNHG12 downregulation induces follicular dysplasia by modulating the glycolysis of granulosa cell in polycystic ovary syndrome
Our findings collectively demonstrate that the SNHG12/HMGB1/PTEN axis serves as a novel regulatory mechanism in PCOS by modulating glycolytic-mediated follicular dysplasia in GCs, offering a potential therapeutic target for PCOS.
Authors
- Bing Qu (ORCID: https://orcid.org/0000-0002-6299-988X)
- Jinli Ding (ORCID: https://orcid.org/0000-0003-4247-3335)
- Qiuji Wu (ORCID: https://orcid.org/0000-0002-4655-3108)
- Yu Chen (ORCID: https://orcid.org/0000-0002-8206-3325)
- Hui Qiu (ORCID: https://orcid.org/0000-0002-9702-3254)
- Sisi Yan (ORCID: https://orcid.org/0009-0003-1342-9973)
Institutions
- Wuhan University (CN)
- Zhongnan Hospital of Wuhan University (CN)
- Renmin Hospital of Wuhan University (CN)
- Wuhan Children's Hospital (CN)
Publication Details
- Journal
- Frontiers in Cell and Developmental Biology
- Published
- 2025-05-23
- DOI
- https://doi.org/10.3389/fcell.2025.1585987
- Primary Topic
- Cancer-related molecular mechanisms research
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Natural Science Foundation of China
- China Postdoctoral Science Foundation
- Department of Science and Technology, Hubei Provincial People's Government
- Fundamental Research Funds for the Central Universities
- Wuhan Science and Technology Project