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Figure 4 | Molecular Cancer

Figure 4

From: Molecular mechanism of cytotoxicity induced by Hsp90-targeted Antp-TPR hybrid peptide in glioblastoma cells

Figure 4

Increase of the erUPR by Antp-TPR peptide. (A) The increase of Bip promoter activation by either Antp-TPR peptide or 17-AAG. GB cells (U251, A172, and SN19) were transfected with pBipPro-Luc and exposed to ER stress. Cells were incubated with or without Antp-TPR peptide or 17-AAG for 18 h after 1 h of treatment with Tg, and then a reporter assay was performed using the Dual-Glo Luciferase assay system as described in the Materials and Methods section. Data represent the mean ± SD (*P < 0.01 compared to control cells without Antp-TPR or 17-AAG). (B) Effect of Antp-TPR peptide on the transcriptional level of Bip and CHOP after induction of the erUPR. Total RNA isolated from GB cells treated with or without Antp-TPR peptide after the induction of the erUPR by Tg treatment was reverse-transcribed to cDNA, and then assessed by PCR (inset) or real-time quantitative PCR using specific primers for Bip and CHOP as described in the Materials and Methods section. GAPDH served as an internal control. Histogram represent the mean ± SD (*P < 0.01 and **P < 0.05 compared to Tg + Antp-TPR 0 μM group, respectively). (C) Effect of Antp-TPR peptide on expression level of Bim after induction of the erUPR. GB cells were treated with or without Antp-TPR peptide after induction of the erUPR by Tg treatment, and then examined by Western-blot analysis to determine the expression level of Bim. Bands were visualized by chemiluminescence and β-actin was used as the loading control.

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