Fig. 3.

Evaluation of the ability of Oxa, Oxa‐ C16, NP1, or NP2 to intervene in CT26 cancer cells by the STING pathway for therapeutically enhanced com bined chemotherapy and immunotherapy. A) Schematic illustration of the mecha nism of action of NP2 to active the STING pathway. B) Change in the expres sion levels of STING pathway associated proteins upon concentration dependent treatment with NP1 determined by Western Blot analysis. C) Change in the expression levels of STING pathway associated proteins upon treatment determined by Western Blot analysis. D) Change in the expression levels of γ‐ H2A u pon treatment determined by Western Blot analysis. E) Comparison of the expr ession levels of γ‐ H2A determined by flow cytometry. Data are means ± SD. ns = no statistical difference, ∗∗∗p < 0.001 determined by ordinary one‐ way A NOVA and Tukey post‐ hoc tests. F) Immunofluorescence confocal laser scanni ng microscopy images of P‐ STING upon treatment. Scale bar = 50 μm. G) Im munofluorescence confocal laser scanning microscopy images of γ‐ H2AX upon treatment. Scale bar = 20 μm. H) Change of IFN‐ β levels upon treatment deter mined by an ELISA assay (n = 3 independent experiments). I) Change of IL‐ 6 levels upon treatment determined by an ELISA assay (n = 3 independent experim ents). J) Maturation of mouse bone marrow‐ derived dendritic cells determined by flow cytometry. H–J) n = 3 independent experiments. Data are means ± SD. ∗p < 0.05, ∗∗p < 0.01 determined by ordinary one‐ way ANOVA and Tukeypost‐ hoc tests. (Reprinted from ref. (95) under the terms and conditions of th e Creative CommonsAttribution (CCBY)license (http://creativecommons.org/licenses/by/4.0/).).