Fig 1: Nomogram for predicting 8- and 5-year overall survival in patients with clear cell renal cell carcinoma. (A) Nomogram for predicting clinical outcomes, integrating T stage, distant metastasis, Fuhrman nuclear grade, necrosis, ECOG PS and tumor CTR1 expression. (B) Calibration plot for predicted and observed 8-year OS rate. (C) Calibration plot for predicted and observed 5-year OS rate. Grey line, ideal model; vertical bars, 95% confidence interval. ECOG PS, Eastern Cooperative Oncology Group performance status; CRT1, copper transporter 1; OS, overall survival.
Fig 2: Dextran-Catechin effect in neuroblastoma xenograft model. Dextran-Catechin decreases tumor growth (A); it improves animal survival (B) without affecting the overall animal weight gain (C). Immunohistochemistry of tumors confirmed downregulation of CTR1 in all the tumors from mice treated with Dextran-Catechin compared to the control group (D); this is evident in the representative pictures of CTR1 staining in a tumor of a control mouse injected with saline (E); and a mouse injected with Dextran-Catechin (F). Data obtained from n=5 animals per group, deviation calculated as SEM (*: p < 0.05; **: p < 0.01).
Fig 3: ZNF711 regulates SLC31A1 promoter activity in EOC cells. (a) The SLC31A1 promoter luciferase reporter plasmids and Renilla pRL-TK plasmids were transfected into the indicated empty vector-transduced, ZNF711-transduced, control shRNA-transduced, and the ZNF711-shRNA transduced HEY and SKOV3 cells. After 48 h, the luciferase signal was examined and presented. (b) Schematic illustration of the P1-P7 cloned fragments of the human SLC31A1 promoter. (c and d) Luciferase activity of the SLC31A1 promoter fragments in control vector cells and ZNF711-overexpressing EOC cells. (e and f). Luciferase activity of SLC31A1 promoter fragments in shRNA control vector cells and ZNF711 knockdown EOC cells. (g) ChIP assays were performed using an anti-Flag antibody to screen three predicted ZNF711-binding sites on the SLC31A1 promoter. IgG was used as a negative control. (h) ChIP assay showing the enrichment of Pol II on region 2 in the SLC31A1 promoter in the indicated HEY and SKOV3 cells. Each bar shown in the figure represents the mean ± SD of three independent experiments. *p < 0.05 (unpaired t-test or one-way ANOVA with Bonferroni's correction).
Fig 4: Dextran-Catechin induced downregulation of GSH in SK-N-BE(2)-C tumor cells. L-BSO was used a positive control of GSH reduction (A). Representative western blot (B) and densitometry analysis (C) showing that the expression of Copper transporter 1 (CTR1) is not reduced by Dextran-Catechin (DC 20µg/mL) in the presence of the proteasome inhibitor MG132 (10µM). Data obtained as mean of at least three experiments, deviation calculated as SEM (**: p < 0.01; ***: p < 0.001; ****: p < 0.0001).
Fig 5: CTR1 expression stratified by SSIGN/SSIGN (localized) score and Kaplan-Meier analyses of OS/DFS. (A) OS and (B) DFS rates of all patients according to CTR1 expression. Relative proportions of CTR1 expression status in three risk groups according to the (C) SSIGN and (D) SSIGN (localized) score. High CTR1 expression rates were elevated as the risks increased. (E) OS and (F) DFS rates of low-risk patients according to CTR1 expression. (G) OS and (H) DFS rates of intermediate/high-risk patients according to CTR1 expression. CTR1, copper transporter 1; SSIGN, Mayo Clinic stage, size, grade and necrosis; OS, overall survival; DFS, disease-free survival.
Supplier Page from Abcam for Anti-SLC31A1 / CTR1 antibody