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已发表论文
m6A 调控因子 METTL3 和 YTHDF2 的鉴定与表征：揭示其在子宫内膜异位症中的生物学功能
Authors Ren C, He Y, Zhao Y, Zhang G
Received 9 July 2025
Accepted for publication 11 October 2025
Published 23 October 2025 Volume 2025:17 Pages 3761—3776
DOI https://doi.org/10.2147/IJWH.S552629
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Vinay Kumar
Chengcheng Ren,1,* Yanan He,1,* Yunlong Zhao,2 Guangmei Zhang1
1Department of Gynecology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People’s Republic of China; 2Plastic Surgery Laser Center, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Guangmei Zhang, Email guangmeizhang2014@163.com
Background: Endometriosis (EMs) is a benign gynecological disorder that exhibits several malignant characteristics, including proliferation and angiogenesis. N6-methyladenosine (m6A) modification plays a crucial role in regulating RNA splicing, subcellular localization, translation and RNA-protein interactions, ensuring precise and timely gene expression. Despite ongoing research, the pathogenesis of EMs remains elusive. This study aimed to investigate the potential roles of m6A regulators N6-adenosine-methyltransferase catalytic subunit (METTL3) and YTH domain family, member 2 (YTHDF2) in the development of EMs.
Methods: We employed a comprehensive approach that combi data from the Gene Expression Omnibus (GEO) database, biological information analysis technologies, and validation using other databases and clinical tissues. This allowed us to uncover aberrantly m6A regulators METTL3 and YTHDF2 and investigate biological functions of EMs.
Results: Our investigation identified METTL3 and YTHDF2 as critical m6A regulators exhibiting significant downregulation in ectopic endometrium samples compared to healthy controls. In vitro of biological behaviors studies demonstrated that METTL3 and YTHDF2 inhibited proliferation, migration, invasion and angiogenesis.
Conclusion: These findings unveil novel insights into m6A modification of EMs, shedding light on potential biomarkers and paving the way for precision medicine approaches in the treatment for EMs.
Keywords: endometriosis, m6A regulators, METTL3, YTHDF2, angiogenesis
1Department of Gynecology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People’s Republic of China; 2Plastic Surgery Laser Center, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Guangmei Zhang, Email guangmeizhang2014@163.com
Background: Endometriosis (EMs) is a benign gynecological disorder that exhibits several malignant characteristics, including proliferation and angiogenesis. N6-methyladenosine (m6A) modification plays a crucial role in regulating RNA splicing, subcellular localization, translation and RNA-protein interactions, ensuring precise and timely gene expression. Despite ongoing research, the pathogenesis of EMs remains elusive. This study aimed to investigate the potential roles of m6A regulators N6-adenosine-methyltransferase catalytic subunit (METTL3) and YTH domain family, member 2 (YTHDF2) in the development of EMs.
Methods: We employed a comprehensive approach that combi data from the Gene Expression Omnibus (GEO) database, biological information analysis technologies, and validation using other databases and clinical tissues. This allowed us to uncover aberrantly m6A regulators METTL3 and YTHDF2 and investigate biological functions of EMs.
Results: Our investigation identified METTL3 and YTHDF2 as critical m6A regulators exhibiting significant downregulation in ectopic endometrium samples compared to healthy controls. In vitro of biological behaviors studies demonstrated that METTL3 and YTHDF2 inhibited proliferation, migration, invasion and angiogenesis.
Conclusion: These findings unveil novel insights into m6A modification of EMs, shedding light on potential biomarkers and paving the way for precision medicine approaches in the treatment for EMs.
Keywords: endometriosis, m6A regulators, METTL3, YTHDF2, angiogenesis