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Fig. 3 | BMC Cancer

Fig. 3

From: Inhibition of PI3K/Akt/mTOR overcomes cisplatin resistance in the triple negative breast cancer cell line HCC38

Fig. 3

NVP-BEZ235 treatment fully restores cisplatin sensitivity in HCC38CisR. a 20 nM NVP-BEZ235 added 48 h prior to cisplatin treatment significantly reduced IC50 of cisplatin in HCC38CisR (p < 0.001) but not in HCC38. b 1 μM KU0063794 or 5 μM LY294002 or their combination significantly reduced IC50 of cisplatin in HCC38CisR (p < 0.001). c Western blot analysis of PARP and cleaved PARP in HCC38CisR used as an indicator of active Caspase 3. For combination of NVP-BEZ235 and cisplatin, 20 nM NVP-BEZ235 was incubated 48 h prior to addition of 3 μM cisplatin for 6 h. d Induction of apoptosis by NVP-BEZ235 and cisplatin. 20 nM NVP-BEZ235 was incubated 24 h prior to addition of 5 μM cisplatin for 6 h followed by 24 h of recovery. Combination of NVP-BEZ235 with cisplatin increased apoptotic nuclei (35.3 ± 3.7%) compared to cisplatin alone (11.4 ± 2.3%) and NVP-BEZ235 alone (4.6 ± 2.0%) (***p < 0.001). e Western blot analysis of p-EGFR, p-IGF1R, and p-Akt in HCC38CisR upon 48 h treatment with 20 nM or 280 nM NVP-BEZ235. f Densitometric analysis of the protein bands of p-EGFR, p-IGF1R, and p-Akt in HCC38 and HCC38CisR were performed using ImageJ software (NIH). Data are means ± SD, n = 3. All values have been normalized to HCC38 control. Statistical analysis was performed using one-way ANOVA test (* p < 0.05, ** p < 0.01, and *** p < 0.001). g Effect of 20 nM or 280 nM NVP-BEZ235 on cell cycle in HCC38CisR. 280 nM NVP-BEZ235 gave a slight but significant (*p < 0.5) reduction of cells in G1 phase (67.3 ± 1.6% vs. 60.0 ± 0.9% in control) accompanied by an increase in cells in G2/M phase (23.6 ± 1.4% vs. 28.3 ± 0.5% in control). All data shown are mean +/− SEM, n = 3, except (C/E) showing a representative experiment out of 3

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