METTL3/YTHDF1 mA axis promotes tumorigenesis by enhancing DDR2 expression in ovarian cancer.

Ovarian cancer has the highest mortality among all gynecological malignancies. Therefore, it is urgent to determine the molecular mechanism of ovarian cancer progression. As the most prevalent modification of messenger RNA (mRNA), N6-Methyladenosine (mA) modification is recognized as a key regulatory role in the progression of various tumors. However, the specific role of mA and its related regulatory pathways in ovarian cancer (OV) remains unclear. In this study, we demonstrated that the METTL3/YTHDF1 mA axis plays an important role in the progression of ovarian cancer. Depletion of METTL3/YTHDF1 impaired cancer proliferation and metastasis in vitro and in vivo. Mechanistically, The METTL3/YTHDF1 m6A axis directly binds to the mRNA of DDR2, thereby promoting the expression levels of the tumor promoter DDR2 and thus contributing to the progression of ovarian cancer. Collectively, our findings on the METTL3/YTHDF1/DDR2 mA axis provide the insight into the underlying mechanism of ovarian carcinogenesis and highlight potential therapeutic targets for cancer treatment.