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. 2020 Jun 11;12(6):1540. doi: 10.3390/cancers12061540

Figure 7.

Figure 7

J2 sensitizes TZMB-resistant cell lines to successfully restore significant anticancer activity of TZMB. (A) The effect of co-treatment with J2 (10 μM) and TZMB (10 μg/mL) on HER2 and its downstream AKT signaling pathway was assessed in three different cell lines, BT-P, BT-TR, and JIMT-1. The HER2 and p-AKT levels were most significantly reduced in the co-treatment group, which also showed enhanced alterations in HSP27 dimerization (12 h treatment of both drugs). (B) Marked reduction in S15 and 78 phosphorylation was observed in the co-treatment group. No changes were found in S8 phosphorylation. The experimental conditions used in (A) were also applied here. (C) The effect of co-treatment with J2 (10 μM) and TZMB (10 μg/mL) on apoptosis signaling was assessed in three different cell lines, BT-P, BT-TR, and JIMT-1. Pro-apoptotic markers in the co-treatment group were significantly upregulated, along with enhanced alterations in HSP27 dimerization (24 h treatment of both drugs) (D) Remarkable synergism of growth inhibitory effect was observed in the group co-treated with J2 and TZMB (48 h treatment of both drugs). ANOVA, *** p < 0.001 versus TZMB-only group. (E) Long-term proliferation rate was also markedly inhibited in the TZMB + J2 group (10-day incubation). ANOVA, *** p < 0.001 versus CON.