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Fig. 6 | Journal of Hematology & Oncology

Fig. 6

From: Inhibition of thioredoxin activates mitophagy and overcomes adaptive bortezomib resistance in multiple myeloma

Fig. 6

Inhibition of thioredoxin decreases mTOR and ERK1/2 phosphorylation. a Genetic interaction network associated with mitophagy and thioredoxin. b Optimized network associated with mitophagy and thioredoxin. In this network, circle represents node (proteins), while line represents edge (connections). c Western blot analysis of mTOR and p-mTOR expression in MM.1R-BTZ-resistant cells treated with BTZ (5 nM) and/or PX12 (2.5 μM) treatment for 48 h. d Western blot analysis of mTOR and p-mTOR expression in RPMI8226/Dox-BTZ-resistant cells treated with BTZ (5 nM) and/or PX12 (2.5 μM) treatment for 48 h. e Western blot analysis of p-ERK1/2 expression in MM.1R-BTZ-resistant cells treated with BTZ (5 nM) and/or PX12 (2.5 μM) for 48 h. f Western blot analysis of p-ERK1/2 expression in RPMI8226/Dox-BTZ-resistant cells treated with BTZ (5 nM) and/or PX12 (2.5 μM) treatment for 48 h. The intensity of expression was semi-quantitated using Image-Pro Plus 6.0 software and adjusted to β-actin. g Cell viability of MM.1R-BTZ-resistant cells treated with BTZ (5 nM) or/and PX12 (2.5 μM) with or without mTOR activator MHY1485 (range from 0.5 to 20 μM). h Cell viability of MM.1R-BTZ-resistant cells treated with BTZ (5 nM) or/and PX12 (2.5 μM) with or without ERK activator tBHQ (range from 0.5 to 20 μM). i Cell viability of RPMI8226/Dox-BTZ-resistant cells treated with BTZ (5 nM) or/and PX12 (2.5 μM) with or without mTOR activator MHY1485 (range from 0.5 to 20 μM). j Cell viability of RPMI8226/Dox-BTZ-resistant cells treated with BTZ (5 nM) or/and PX12 (2.5 μM) with or without ERK activator tBHQ (range from 0.5 to 20 μM). Each experiments were repeated three times. Error bars, standard error of the mean (SEM); *p < 0.05, **p < 0.01, ***p < 0.005, ****p < 0.001

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