GATAD2B promotes ovarian cancer malignant progression via MYC/CD47 Axis.

This study elucidates the biological function of GADAT2B and its underlying mechanism in ovarian cancer.The results of our experiment showed that GATAD2B highly expressed in OC tissues, which was associated with a poor prognosis. METTL3 regulated the expression of GATAD2B in OC cells via m6A methylation. And it was unveiled that up-regulation of GATAD2B significantly promoted OC growth, invasion, migration of and suppressed the tumor cell apoptosis. After transfected with sh-GATAD2B, the OC cells were just the reverse in behavior. Additionally, GATAD2B played a crucial role in regulating CD47 expression via the MYC-mediated pathway, and the further experiments showed that GATAD2B and MYC were co-localized on tumor cell membrane. The in vivo and in vitro experiments showed an important role of GATAD2B in OC growth and metastasis, as confirmed by the inhibited tumor growth and the enhanced M1 macrophage infiltration.GATAD2B m6A methylation mediated by METTL3 can promote malignant progress. And GATAD2B can promote immune escape by MYC/CD47 pathway in OC, providing a promising anti-OC therapeutic target.