Fig. 2: Hyperactive mTORC1 sensitizes MM to PIs independently of autophagy.
From: An mTORC1 to HRI signaling axis promotes cytotoxicity of proteasome inhibitors in multiple myeloma
A MM cells were treated with IXZ [20 nM] for 48 h. Shown is average relative viability of three independent experiment ± S.E.M., *p < 0.05 of unpaired two-tailed student’s t-test. B Cells were treated as described in (A) followed by immunoblotting analysis of cleaved caspase3 for apoptosis assessment and p97 as a loading control. Shown is a technical duplicate for each condition. C MM cells were incubated in hypoxia for 48 h. Shown is average relative viability of three independent experiment ± S.E.M., *p < 0.05 of unpaired two-tailed student’s t-test. D Cells were incubated as described in (C) followed by immunoblotting analysis of cleaved caspase3 for apoptosis assessment and p97 as a loading control. Shown is a technical duplicate for each condition. E MM cells were treated with IXZ [40 nM] for 24 h in either normoxia or hypoxia as indicated. Shown is average relative viability of three independent experiment ± S.E.M., *p < 0.05 of unpaired two-tailed student’s t-test. ns, not significant. F A time-response analysis of mTORC1 and autophagy activities following IXZ [32 nM] treatment in wt versus ATG7 KO MM.1S cells. Inhibition of autophagy was confirmed by immunoblotting for p62 and LC3BI/II proteins. Shown is a typical immunoblots out of three independent experiments. G MM cells were treated with IXZ [20 nM] for 48 h. Shown is the average relative viability of three independent experiment ± S.E.M., ns, not significant.
