Identification and Characterization of m6A Regulators METTL3 and YTHDF2: Unveiling Their Biological Functions in Endometriosis

Ren C, He Y, Zhao Y, Zhang G
2025 · W7094977598
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This study investigated the roles of m6A RNA modification regulators METTL3 and YTHDF2 in endometriosis by integrating analyses of publicly available Gene Expression Omnibus (GEO) data with biological information analyses, cross-database validation, and comparisons with clinical tissue samples. The authors identified METTL3 and YTHDF2 as critical m6A regulators that were significantly downregulated in ectopic endometrium versus healthy controls. In vitro functional assays reported that METTL3 and YTHDF2 inhibited proliferation, migration, invasion, and angiogenesis, and the paper frames these results as mechanistic links between m6A dysregulation and disease biology. This paper is centrally about endometriosis — specifically, it characterizes METTL3 and YTHDF2 as downregulated m6A regulators affecting proliferation, invasion, and angiogenesis in ectopic endometrial tissue.

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Abstract

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 workCorrespondence: Guangmei Zhang, Email [email protected]: 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
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International Journal of Women's Health (Oct 2025) Identification and Characterization of m6A Regulators METTL3 and YTHDF2: Unveiling Their Biological Functions in Endometriosis Abstract 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 workCorrespondence: Guangmei Zhang, Email [email protected]: 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

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