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

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.