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. 2025 Aug 22;14:109. doi: 10.1186/s40164-025-00700-0

Fig. 2.

Fig. 2

Triapine stimulates FAS upregulation via ER stress and NFκB. (A) Expression of receptor genes in SW480 cells (1 µM Triapine, 18 h). Values are mean log fold change compared to control. (B) Representative flow cytometry histograms and quantification (mean fluorescence intensities (MFI) ± SD) of FAS expression of Triapine-treated CT-26 cells. (C) Representative IHC images (scale bar: 100 μm) and (D) associated quantification of FAS expression (mean % ± SEM) in CT-26 tumors after treatment with Triapine. (E) Caspase 8 activity and (F) cell viability of HCT116 cells after 24 h Triapine preincubation, followed by 24 h FASL treatment. Values are mean ± SD from one representative experiment out of three, normalized to untreated control. (G) Impact of the ER-stress inhibitor 4-PhB on Triapine-induced NFκB activity was analyzed using NFκB reporter HEK293-Blue™ hTLR7 cells after 24 h. Values are mean ± SD of three independent experiments normalized to control and cell number. Impact of (H) 4-PhB or ± (I) Bay 11-7082 on Triapine-induced FAS expression in HCT116 cells with functional caspase 8 signaling after 24 h treatment. Values are MFI ± SD of three independent experiments, normalized to control. Significance was determined by one-way, two-way ANOVA with Bonferroni´s or Dunnett´s multiple comparisons test or unpaired T-test (**** p < 0.001, *** p < 0.001, ** p < 0.01, * p < 0.05). (J) Scheme summarizing the immune-enhancing activities of Triapine via induction of ICD and FAS upregulation.