Fig. 5: METTL3 controls MEG3 levels in a YTDC1-dependent fashion in the context of RILI.

A Confirmation of the establishment of YTHDC1-knockdown BNL CL2 cells (**P < 0.01). B MEG3 expression in BNL CL2 cells was analyzed via qPCR in YTHDC1 knockdown cells (**P < 0.01). C. MEG3 expression levels were analyzed via qPCR following YTHDC1 knockdown and irradiation in BNL CL2 cells (**P < 0.01). D, E RIP assays were used to pull down MEG3 with anti-YTHDC1 in BNL CL2 cells following METTL3 knockdown and irradiation (**P < 0.01). F MEG3 levels were assessed in cells in which METTL3 had been knocked down and co-transfected with TYHDC1 with or without irradiation (**P < 0.01). G MEG3 levels were detected in NC or YTHDC1 shRNA-treated cells by qPCR following actinomycin D (1 µg/ml) treatment for the indicated periods (**P < 0.01). H MEG3 and YTHDC1 target binding sites. I YTHDC1 can recognize METTL3-mediated MEG3-m6A modification. J RIP experimental overview. A–G, n = 3. A–G were performed by two-tailed unpaired T-test.