卵巢癌
癌变
癌症研究
转移
癌症
信使核糖核酸
机制(生物学)
肿瘤进展
生物
医学
内科学
基因
生物化学
认识论
哲学
作者
Duo Zhi,Kun Zhou,Shuang Liu,Wen Yu,Mei Dong,Caichuan Yan
标识
DOI:10.1016/j.prp.2023.155047
摘要
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 (m6A) modification is recognized as a key regulatory role in the progression of various tumors. However, the specific role of m6A and its related regulatory pathways in ovarian cancer (OV) remains unclear. In this study, we demonstrated that the METTL3/YTHDF1 m6A 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 m6A axis provide the insight into the underlying mechanism of ovarian carcinogenesis and highlight potential therapeutic targets for cancer treatment.
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