Fig 1: Overexpression of ASPP2 leads to an enhancement in the apoptosis of TRAIL-induced cervical cancer cells via inhibiting autophagy. (A and B) TUNEL staining was performed to verify the effect of ASPP2 on the apoptosis of TRAIL-induced c-33A cells. (C) Expression levels of DR4 and DR5 were detected by western blot analysis. *P<0.05, **P<0.01 and ***P<0.001 vs. control; ###P<0.001 vs. Ov-ASPP2; ∆∆∆P<0.001 vs. Ov-ASPP2 + TRAIL. TRAIL, TNF-related apoptosis-inducing ligand; ASPP2, p53 apoptosis-stimulating protein 2; Ov-ASPP2, overexpression of ASPP2; Ov-NC, overexpression-NC; DR, death receptor.
Fig 2: Engineered macrophages induce the M1 antitumor phenotype in macrophages by autocrine delivery of TRAIL to activate the DR4 receptor. (A) Flow cytometry analysis of CD206 expression in engineered murine RAW264.7 macrophages with and without tumor-conditioned medium (4T1); (B) Quantification of surface marker expression levels of CD206 on macrophages under different conditions (NC, Mono-TRAIL-M, Tri-TRAIL-M), with or without tumor conditioned medium (TCM) stimulation. (C) Flow cytometry analysis of CD86 expression in engineered murine RAW264.7 macrophages with and without tumor-conditioned medium (4T1); (D) Quantification of surface marker expression levels of CD86 on macrophages under different conditions (NC, Mono-TRAIL-M, Tri-TRAIL-M), with or without TCM stimulation. (E) Relative mRNA expression of TNF-α, IL-6, IL-1β, IL-10, TGF-β, and Arginase-1; (F) Western blot analysis the protein expression of DR4 and DR5 in murine Mono-TRAIL-M and Tri-TRAIL-M; G and H. Flow cytometry analysis the protein expression of DR4 and DR5 in murine Mono-TRAIL-M and Tri-TRAIL-M. All experiments were independently repeated three times, and representative results are shown
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