Abstract
RNA epigenetic modification take part in many biology processes, and the N6-methyladenosine (m6A) methylation of specific mRNAs in endometrial cancer (EC) tissues play a key role in regulating the tumorigenicity of EC, but the specific mechanism still unknown and need to be investigated in the future. Here, we found that m6A reader protein YTHDF2 expression was significantly upregulated in EC compare to tumor adjacent tissues, YTHDF2 was then identified to inhibit the proliferation and invasion of EC cell lines. Mechanistically, the m6A reader YTHDF2 bind the methylation sites of target transcripts IRS1 and promoted IRS1 mRNA degradation, consequently inhibiting the expression of IRS1 and inhibiting IRS1/AKT signaling pathway, finally inhibit the tumorigenicity of EC. Thus, we demonstrated that YTHDF2 inhibited the proliferation and invasion of EC via inhibiting IRS1 expression in m6A epigenetic way, which suggests a potential therapeutic target for EC.