Fig. 1
From: The therapeutic potential of pegylated arginase I treatment in glioblastoma
Glioblastoma lacks arginine-replenishing enzymes and is chemo-sensitive to BCT-100. (a) Arginine metabolism. The green arrows indicate the urea cycle pathway. The red arrow indicates the arginine–nitric oxide pathway. The blue arrow indicates arginine breakdown by arginine deiminase. (b) RNAseq data from dataset mRNA325 of Chinese Glioma Genome Atlas of 85 first-diagnosed glioblastoma patients showing gene expression of GAPDH, OTC, and ASS1 as FPKM (fragments per kilobase of transcript per million mapped reads). (c) Western blotting analysis of OTC and ASS1 expression in four glioblastoma cell lines: U87, U373, U138, and D54. Mouse liver extract was used as the positive control. GAPDH was used as the loading control. The blots originated from the same protein extract separated by different gels and transferred to different blots. Such an arrangement was used because of the similar sizes of OTC, ASS1, and GAPDH, and stripping could not make the protein bands clearly distinguishable. The whole blots of Fig. (c(i)), (c(ii)), and (c(iii)) are shown in Supplementary Fig. S1a, S1b, and S1c, respectively. (d) (i-iv) Dose–response curve (in terms of cellular activities) of U87, U373, U138, and D54 (representative results presented with technical triplicates) treated with different concentrations of BCT-100, respectively, by using XTT assay. ***p < 0.001 compared to PBS. (d) Cytotoxicity responses of U87, U373, U138, and D54 treated with or without 1 U/ml BCT-100 and/or 40 µM citrulline by using annexin V/propidium iodide assay. *p < 0.05 compared to PBS. ***p < 0.001 compared to the PBS.
