RBM10 loss confers growth advantage in vitro and AS targets of RBM10. (A) Cell proliferation in RBM10-mutant thyroid cancer cells (PE121410 and KTC1) following expression of RBM10; effects of RBM10 silencing on growth of RBM10 WT thyroid cancer cell lines (SW1736 and 8305C). (B) RBM10-dependent AS genes common to five isogenic ± RBM10 thyroid cancer cells. (C and D) IGV view of exon junctions in the RNAseq data of the indicated cells showing inclusion of exon 19 of VCL (C) and exons 8 +13–15 of CD44 genes (D) in RBM10 mutant PE121410 and KTC1 cells and their exclusion following RBM10 expression, with reciprocal changes in RBM10-KD 8305C cells. (E) Scheme showing exon structure of VCL, CD44, and TNC genes. (F) RBM10-targeted exon inclusion (red) isoforms of VCL, CD44, and TNC spliced-in with adjacent constitutive exons (green). PE par: parental PE121410; KTC par: KTC1 parental. (G) IGV plot displaying RBM10 PAR-CLIP data from HEK293 cells (Wang et al., 2013) showing CLIP-tags (dark blue) over the gene body of VCL pointing to RBM10-binding peaks (light blue arrow) bracketing exon 19. The IGV plot show RBM10-CLIPs from two-replicates (RBM10Wang2013a and RBM10Wang2013b downloaded from https://dorina.mdc-berlin.de/). (H and I) Data from RBM10 eCLIP study performed in MOLM13 AML cells (Wang et al., 2023) showing coverage plots for CLIP peaks (both input control and RBM10 IP) over the gene body of VCL (H) and CD44 (I). The graphs show mean coverage over four replicates with a raster plot (red) marking significant RBM10 peaks. IGV: Integrative Genomics Viewer.