Fig 2: DNA methylation modifications the RBM14 promoter. A MEXPRESS view of the TCGA data for RBM14 gene in LUAD. B The promoter methylation level of RBM14 gene was analyzed by UALCAN using TCGA LUAD dataset. C The promoter methylation level of RBM14 gene in lung cancer cell lines after 5-aza-dC treatment. *p <0.05 vs DMSO. Three independent experiments were performed

Fig 3: Paraspeckle upregulation in macrophages sequesters nuclear RNA-binding proteins. (A) RNA-FISH of Neat1 (red) and immunofluorescence staining of PSP1 (green) in RAW 264.7 macrophages at 0.5 h and 1 h post-LPS treatment (100 ng/mL). Correlation coefficient between Neat1 and PSP1 quantified below. (B) As in (A) but for SFPQ. (C) As in (A) but for FUS. (D) As in (A) but for RBM14. (E) As in (A) but for NONO. (F) As in (A) but for hnRNP M. Statistical tests: Data are presented as the mean n = 3 unless otherwise noted. Statistical significance was determined using a one-way ANOVA. *P < 0.05, **P < 0.01, ***P < 0.001.

Fig 4: RBM14 as an ARGOS gene.a The map of copy number alterations in chromosome 11 shows a focal amplification, where RBM14 is located next to CCND1. Amplifications (red) and deletions (blue) are shown for this genomic region. The genomic location of OGs and TSGs are shown at the level of amplification- and deletion frequencies for easier visibility, reflecting their respective selection pressure. b Compensation or ORF dropout scores for RBM14 in our pan-cancer analysis (green) as well as in breast (purple) and lung (orange) lineages chosen for downstream functional validation. Bars represent the mean, error bars the standard deviation of the posterior. c Depletion scores for RBM14 ORFs across 17 independent screens, including breast (BRCA), ovarian (OV), neuroblastoma (NB), skin cutaneous melanoma (SKCM), lung adenocarcinoma (LUAD), Ewing sarcoma (EWS), medulloblastoma (MB) and prostate adenocarcinoma (PRAD) cell lines. The mean log-fold change in growth is shown as a line for each tumor type. d Lung and breast cancer cell lines chosen for functional validation based on their gene expression and DNA copy number profile on CCLE. e RBM14 overexpression leads to a growth inhibition phenotype. The mean and S.D. of three replicates are shown. Data was analyzed using two-way ANOVA. f RBM14 overexpressing lung and breast cells show a decrease in nascent protein synthesis. Fluorescence (GFP; green) is quantified relative to cell number (DAPI; blue). Luciferase overexpressing cells were used as a control. Scale bar: 100 µM. Mean +/− SD is shown from two biological replicates (five images per cell line; six for HCC70) and analyzed by unpaired two-tailed t test. g The fraction of apoptotic cells following RBM14 overexpression was determined by flow cytometry-based quantification of annexin V and PI-positive cells. The mean and S.D. of three replicates is shown. Data was analyzed by unpaired two-tailed t test. Source data for Fig. 5c, f, and g are provided as Source Data files.

Fig 5: Effects of RBM14 MO on the maturation of mouse oocytes. (A) Western blot analysis verified the efficiency of endogenous RBM14 knockdown. (B) RBM14 band intensities normalized to α-tubulin. (C) Representative bright-field images of RBM14-MO injected and control oocytes. Black rhombuses: successful polar body extrusion in control oocytes; black arrow: oocyte with apparent symmetric division; black asterisk: oocyte failed to extrude a polar body. Scale bar = 200 μm. (D) Rate of GVBD in control and RBM14-MO injected oocytes. (E) Rate of polar body extrusion in control and RBM14-MO injected oocytes. (F) Rate of symmetric division in control and RBM14-MO injected oocytes. A total of 364 control oocytes and 332 RBM14-MO injected oocytes were analyzed. Data are mean ± SEM of three independent experiments. NS, not significant, *P < 0.05 and **P < 0.01.