Fig 2: Nup210 is dispensable for muscle growth and survival.(A) Total protein was isolated from control and Nup210 knockout quad muscle and Nup210 levels were analyzed by Western blots. Hsp90 was used as loading control. (B) Weight measurements of Nup210+/+ and Nup210−/− mice (n = 14–15) were taken every 2 wk. (C) Kaplan–Meier plot of Nup210+/+ and Nup210−/− mice (n = 19–20) measuring survival for up to 25 mo. (D) Fresh tissue weights for Quad and TA muscles isolated from Nup210+/+ and Nup210−/− mice (n = 3). Data are plotted as mean ± SEM.

Fig 3: Nup210 levels increase in regenerating muscle fibers.Sections from uninjured and BaCl2 injured TA muscles were stained for Nup210 (green) and Hoechst (Blue). Scale bar, 25 μM.

Fig 4: Primary muscle satellite cells from Nup210 knockout mice efficiently differentiate into myotubes.(A) Schematic illustration (top) and representative images immunofluorescence staining (bottom) of sorted satellite cells from Nup210+/+ and Nup210−/− mice after induction of myogenic differentiation. Arrows indicate undifferentiated muscle progenitor cells which lack Nup210 expression. Scale bar, 50 μm. (B) Representative immunofluorescence images of differentiated satellite cells from Nup210+/+ and Nup210−/− mice stained for myosin heavy chain (MHC) and Hoechst. Scale bar, 300 μm. (C) Nup210+/+ and Nup210−/− satellite cells were sorted, differentiated, and stained for MHC. The percentage of nuclei in MHC-positive cells (differentiation index) was quantified. (D) Nup210+/+/Pax7-CreERT2 and Nup210f/f/Pax7-CreERT2 were treated with tamoxifen and satellite cells were isolated and differentiated in vitro. (C) The differentiation index (percentage of nuclei in MHC-positive cells) was quantified as in (C). (D, E) Representative immunofluorescence images of cells from (D) stained for Nup210 and MHC. Scale bar, 100 μm. Data are plotted as mean ± SD.

Fig 5: NUP210 expression in clinical datasets. (A) Epigenetic status around NUP210. AR binding to NUP210 in DHT stimulated LNCaP and AR/AR-V7 binding in LNCaP95 in the absence and presence of DHT were shown. (B) RNA expression of NUP210. AR-V7 knockdown decreased FPKM value of NUP210. (C) FAIRE-qPCR analysis at AR/AR-V7 target region around NUP210 in hormone-depleted or -stimulated LNCaP and hormone-depleted LNCaP95. (D) RT-qPCR analysis of NUP210 in LNCaP and LNCaP95 cells with/without shRNA treatment. (E) Reduction of H3K27ac level at the NUP210 enhancer. H3K27ac enrichment was measured by ChIP-qPCR at the AR/AR-V7 target region around NUP210, showing a decrease following AR-V7 knockdown. Data represent the mean ± SEM of 3 experiments. (F)NUP210 expression levels in benign lesions, primary PC, and CRPC (Grasso prostate dataset). Expression of NUP210 was elevated in primary PC compared with benign lesions (P=0.001), but markedly upregulated in CRPC (P=2 × 10−11). (G)NUP210 expression levels in PC cases with higher and lower expression of AR-V7 (TCGA PRAD dataset). Among the 550 patients enrolled in TCGA, the top 100 patients showing high expression of AR-V7 and the bottom 100 patients showing low expression of AR-V7 are defined as AR-V7 high and low groups, respectively.