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. 2020 May;9(5):3416–3425. doi: 10.21037/tcr-19-2246

Figure 5.

Figure 5

TEXs maintain renal carcinoma cells drug resistance via mTOR-ERK-STAT-NF-κB signal pathways. (A) Exosome detection. Both CD63 and ALIX are markers of exosome, VDAC1 is marker of mitochondrial. (B) ACHN cells were treated with PBS, 5 µM IFNα, 10 µg/mL 769-P exosomes, and 5 µM IFNα + 10 µg/mL 769-P exosomes, respectively. (C) ACHN cells were treated with PBS, 5 µM BP-1-102, 10 µg/mL 769-P exosomes, and 5 µM BP-1-102 + 10 µg/mL 769-P exosomes, respectively. (D) ACHN cells were treated with PBS, 2.5 µM rapamycin, 10 µg/mL 769-P exosomes, and 2.5 µM rapamycin + 10 µg/mL 769-P exosomes, respectively. All statistical data were expressed with mean ± SEM. Data were analyzed via Student’s t-test or one-way ANOVA, p value less than 0.05 was considered significant. *, P<0.05; ***, P<0.001, all compared with control group. TEXs, tumor derived exosomes; SEM, standard error of the mean.