ER stress mediates postslippage AMPK activation.

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ER stress mediates postslippage AMPK activation. ER stress mediates postslippage AMPK activation. A, U2OS cells were treated with nocodazole (Noc) or paclitaxel (PTX) for the indicated duration. Lysates from mitotic cells (M) or postslippage cells (PS) were subjected to IB and probed for ER stress–related markers. The respective signal intensity ratios are shown at the bottom of the relevant lanes. B and C, U2OS cells were treated with nocodazole or paclitaxel for the indicated time points. Cells were treated with 1 μg/mL tunicamycin (TM) for 24 hours as a positive control. Relative CHOP expression and splicing of XBP1 mRNA was detected by RT-PCR and quantified by qRT-PCR. D, U2OS cells were treated with nocodazole in absence or presence of 10 μmol/L PERK inhibitor (PERKi; GSK2656157), subjected to IB and probed for autophagy-related markers. E, U2OS cells were treated with nocodazole in absence or presence of 10 μmol/L IRE1 inhibitor (IRE1i; 4μ8C), were collected at the indicated time points and analyzed by IB with the indicated antibodies. All data are mean ± SD of three independent experiments (*, P < 0.05; **, P < 0.005; ***, P < 0.001 by Student t test). Rekha Jakhar et al. Mol Cancer Res 2018;16:1625-1640 ©2018 by American Association for Cancer Research