YTHDF3 Promotes N6‐Methyladenosine Modification of SOCS1 to Inhibit JAK1/STAT3 Pathway in the Pathogenesis of Preeclampsia

Preeclampsia (PE) is a common complication during pregnancy. Trophoblast cells are the main cell type of the placenta, and abnormalities in proliferation and differentiation cause anterior placental accretion and lead to the development of PE. This study will investigate the function and related mechanism of N6‐methyladenosine (m 6 A) reader YTH N6‐methyladenosine RNA binding protein F3 (YTHDF3) in PE and provide a rationale for the therapeutic treatment of PE. In the study, YTHDF3 and suppressor of cytokine signaling 1 (SOCS1) expression were significantly upregulated within PE placental tissue samples. YTHDF3 knockdown promoted the capacity of hypoxia‐treated trophoblast cells to proliferate, migrate, invade, and undergo epithelial‐mesenchymal transition (EMT) and inhibited apoptosis. The JAK1/STAT3 pathway is aberrantly activated in trophoblast cells of PE. YTHDF3 binds m 6 A‐modified SOCS1 mRNA to enhance its stability and translation. YTHDF3 / SOCS1 promotes disease progression in PE by inhibiting the JAK1/STAT3 signaling pathway. In conclusion, YTHDF3 promotes the disease progression of PE by enhancing the m 6 A modification of SOCS1 mRNA and suppressing the JAK1/STAT3 signaling pathway. YTHDF3 has been identified as an underlying target for the clinical treatment of PE.