Fig. 2: Cancer cells mediate PDIA1 homeostasis through EV release. | Oncogene

Fig. 2: Cancer cells mediate PDIA1 homeostasis through EV release.

From: Protein disulfide isomerase-enriched extracellular vesicles from bladder cancer cells support tumor survival and malignant transformation in the bladder

Fig. 2

A Western blot showing PDIA1 levels in whole cell lysates and EVs derived from non-transformed SV-HUC and TCCSUP cancer cells with tunicamycin (140 nM Tun; in DMSO) or vehicle control (DMSO) treatment. CD9 was used as an EV marker and normalization control for EV proteins. B Immunofluorescence staining demonstrating PDIA1 and TSG101 intensity and cellular localization in SV-HUC, TCCSUP, and J82 cancer cells with tunicamycin (140 nM Tun) or vehicle (0 nM Tun) treatment. Scale bars: 10 µm. C The percentage of reduced PDIA1 in TCCSUP cancer cells (left) or SV-HUC non-transformed cells (right) with tunicamycin (140 nM Tun) or vehicle (0 nM Tun) treatment as shown by reduced thiol quantification. D Percentage of reduced and oxidized PDIA1 in TCCSUP EVs as estimated by reduced thiol quantification. E EV release kinetics for SV-HUC and TCCSUP cells following tunicamycin (140 nM Tun) or vehicle (0 nM Tun) treatment for 36 h. For (C) and (E), two-way ANOVAs were performed with Fisher’s LSD multiple comparison test; for (C), n = 3, and for (E), n = 9; error bars indicate means ± standard deviation. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. EV extracellular vesicle, PDIA1 protein disulfide isomerase A1, CD9 cluster of differentiation 9, TSG101 tumor susceptibility gene 101, ANOVA analysis of variance, DMSO dimethyl sulfoxide, Tun tunicamycin.

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