Fig 1: Association between CRM1 expression of tumor tissues and differentiation degree. CRM1, chromosome region maintenance 1; IOD, immunohistochemical optical density. *P<0.05, vs. moderate.
Fig 2: Inhibition of nuclear export causes loss in the cytoplasm and accumulation in the nucleus of TET2. a IHC analysis of TET2 after treatment of the SI-NET cell lines CNDT2.5 (adhesive cells) and KRJ-I (suspension cells) with the exportin-1 (XPO1/CRM1) inhibitor leptomycin B. Scale bar, 50 µm. Nuclear accumulation of TET2 is seen. Small labeled dots in the treated KRJ-I cells constitute cellular debris. b Western blot analysis of cytoplasmic and nuclear protein extracts from CNDT2.5 and KRJ-I cells after leptomycin B treatment. Induced absence in the cytoplasm and nuclear retention of TET2 is seen. ß-tubulin and lamin A/C was used as marker for the cytoplasm and nucleus, respectively. c Real-time RT-PCR of XPO1 in paired primary SI-NETs (n = 19) and metastases (n = 22). Normal tissues from the small intestine (n = 3) was arbitrarily used for comparison. A representative overall positively XPO1 stained metastatic tumor is shown to the right. Scale bar, 100 µm
Fig 3: TLNC1 represses nuclear translocation of p53 through interaction with TPR. a p53 expression in indicated SK-Hep1 and HCCLM3 cells, as detected by an immunofluorescence assay. The merged images show overlays of p53 (green) and nuclear staining by DAPI (blue); scale bar: 20 µm. b Immunoblot analysis of p53 in indicated SK-Hep1 and HCCLM3 cells. c p53 expression in cytoplasmic and nuclear fractions, as detected by immunoblot analysis. GAPDH was used as a loading control for the cytoplasmic fraction, and PARP was used as a loading control for the nuclear fraction. d Co-immunoprecipitation among TPR, CRM1 and p53 in SK-Hep1 and HCCLM3 cells, as detected by immunoblot analysis. e Co-immunoprecipitation among TPR, CRM1 and p53 in indicated SK-Hep1 (TLNC1 overexpression) and HCCLM3 (TLNC1 knockdown) cells, as detected by immunoblot analysis. f Co-immunoprecipitation among recombinant TPR, CRM1 and p53 proteins, as detected by immunoblot analysis. The data are the representative of three independent experiments. g Surface plasmon resonance analysis of the binding of CRM1 with increasing concentrations of recombinant TPR in the presence or absence of TLNC1
Fig 4: Association between CRM1 expression of adjacent normal tissues and diameter. CRM1, chromosome region maintenance 1; IOD, immunohistochemical optical density. *P<0.05, vs. =5 cm.
Fig 5: Immunohistochemical analysis of CRM1 expression in (A) adjacent normal control and (B) tumor tissues, in the low differentiation group. (C) CRM1 expression was higher in the adjacent normal tissues compared with the tumor tissues (low differentiation group). CRM1, chromosome region maintenance 1; IOD, immunohistochemical optical density. *P<0.05, vs. tumor tissues.
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