Fig. 4

METTL16 downregulates RAB11B-AS1 through inducing m⁶A modification of RAB11B-AS1. A RAB11B-AS1 expression in SNU-398 and HepG2 cells with METTL16 overexpression or control was detected by RT-qPCR. B RAB11B-AS1 expression in SNU-398 and HepG2 cells with METTL16 knockdown or control was detected by RT-qPCR. C RIP assays were performed in SNU-398 and HepG2 cells to enrich the RNA bound by METTL16, followed by RT-qPCR to detect the enrichment of RAB11B-AS1. D CLIP assays were performed in SNU-398 and HepG2 cells to enrich the RNA directly bound by METTL16, followed by RT-qPCR to detect the enrichment of RAB11B-AS1. E MeRIP assays were performed in SNU-398 and HepG2 cells with METTL16 overexpression or control to enrich m⁶A modified RNA, followed by RT-qPCR to assess m⁶A modification level of RAB11B-AS1, MAT2A, and EEF1A1. F MeRIP assays were performed in SNU-398 and HepG2 cells with METTL16 knockdown or control to enrich m⁶A modified RNA, followed by RT-qPCR to assess m⁶A modification level of RAB11B-AS1, MAT2A, and EEF1A1. G The stability of RAB11B-AS1 over time was measured after blocking new RNA synthesis with α-amanitin (50 µM) in SNU-398 and HepG2 cells with METTL16 overexpression or control. H The stability of RAB11B-AS1 over time was measured after blocking new RNA synthesis with α-amanitin (50 µM) in SNU-398 and HepG2 cells with METTL16 knockdown or control. Results are shown as mean ± SD of n = 3 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 by Student’s t-test (A, C, D, E, G) or one-way ANOVA followed by Dunnett’s multiple comparisons test (B, F, H)