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Fig. 4 | Cell Communication and Signaling

Fig. 4

From: Repurposing thioridazine for inducing immunogenic cell death in colorectal cancer via eIF2α/ATF4/CHOP and secretory autophagy pathways

Fig. 4

Blocking autophagosomes formation could inhibit the thioridazine-induced effect on the release of ICD markers. A Western blot representing knock down of ATG7 protein in CT26 cells. B CT26 cells with deficient ATG7 exhibited compromised autophagosomes formation under thiostrepton (TST) or THD treatment. ICD markers were detected (C) ATP and (D) calreticulin (CRT) in ATG7 KD cell following drug treatment via ATP detection assay and flow cytometry, respectively. E Number of secreted extracellular vesicles in HT29 cells were detected via Nanoparticles Tracking Analysis software (NanoSight NS300, Malvern Panalytical Ltd., Malvern, UK) after THD treatment for 24 h. F SW480 cells with intact ATG5 and ATG5 knockout were treated with THD at the concentrations of 10 and 15 μM for 24 h. The protein levels of ER stress eIF2α/ATF4/CHOP pathway components were examined using western blotting. Data are mean ± SD (N = 3). *: p < 0.05; **: p < 0.01; ***: p < 0.001

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