Fig. 1.

Tumor hypoxia up-regulates GPx1 expression and function in glioblastoma.

(A–C) Enzyme activities of Catalase (CAT), peroxiredoxin (Prx), and glutathione peroxidase (GPx) in the human glioblastoma cells (GBM8401 and U251) and primary glioblastoma cells (GBM04T and GBM09T) at 24 h after normoxic and hypoxic treatment (<1% O₂). (D–E) mRNA levels of GPx1 or GPx3 in the GBM8401, U251, GBM04T, and GBM09T cells at 24 h after normoxic and hypoxic treatment (<1% O₂). (F) Protein levels of GPx1 or GPx3 in the GBM8401 and GBM04T cells at 24 h after normoxic and hypoxic treatment (<1% O₂). (G) Protein levels of GPx1 in the GBM8401 and GBM04T cells at 24 h after normoxia (N), non-interrupted (C.H.) hypoxia (<1% O₂), and cycling (Cy.H.) hypoxia (<1% O₂). (H) Immunostaining of GPx1 expression in hypoxic tumor subpopulations from GBM8401 xenografts. White color represents the colocalization of pimonidazole (green), Hoechst 33342 (blue), and GPx1 (red). (I) GPx1 mRNA levels in normoxic cells (Hoechst 33342⁺ and GFP⁻), chronic hypoxic cells (Hoechst 33342⁻ and GFP⁺), and cycling hypoxic cells (Hoechst 33342⁺ and GFP⁺) isolated from disaggregated GBM8401/hif-1-r and U87/hif-1-r xenografts. Error bars, SD within triplicate experiments. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001, compared with normoxia. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)