Figure 5.

IGF2BP3 promotes MALAT1 nuclear-cytoplasmic shuttling in a m6A‑dependent manner. HepG2.2.15 cells and HBx-expressing HepG2 cells were used for experiments, whereas HepG2 cells and HepG2-NC cells served as controls. A Representative images of FISH assays identifying the subcellular location of MALAT1 (red) in the cells. Scale bars: 20 μm. B The subcellular distribution of MALAT1 was analyzed via qRT-PCR in the cells. U6 and GAPDH were used as nuclear and cytoplasmic markers, respectively. C-D The subcellular distribution of MALAT1 was analyzed via qRT-PCR in the cells transfected with the indicated plasmids. E sgGSEA of IGF2BP3 in the TCGA-LIHC cohort. NES, normalized enrichment score. F The protein level of IGF2BP3 was detected by WB in the cytoplasmic and nuclear fractions of the cells. G RNA pulldown assays were conducted, and IGF2BP3 was pulled down by biotin-labeled sense MALAT1 (S) but not by MALAT1 antisense (AS) RNA in the cytoplasmic and nuclear fractions of the cells. H The subcellular distribution of MALAT1 was analyzed via qRT-PCR in the cells transfected with the indicated plasmids. I-J RNA decay assays showing the effect of overexpressing and knocking down IGF2BP3 on MALAT1 RNA half-life in the cells.