Fig. 2: GBM neurospheres/GSCs are sensitive for Tg that is accompanied by UPR activation. | Cell Death & Disease

Fig. 2: GBM neurospheres/GSCs are sensitive for Tg that is accompanied by UPR activation.

From: ER stress and UPR activation in glioblastoma: identification of a noncanonical PERK mechanism regulating GBM stem cells through SOX2 modulation

Fig. 2

a GBM Nsp cells were treated with different doses of Tg for 24 or 48 h. Cell viability was evaluated by MTS assays. Dose and time-dependent cytotoxicity was observed. b Preformed GG16 and GSC23 Nsp were exposed to Tg for 24 h. Phase contrast microscopy (×10) showed strong toxicity as indicated by Nsp disintegration and debris. c MTS assays of Nsp cells treated with combinations of Tg and the pan-caspase inhibitor Z-VAD, the RIPK1 inhibitor Nec-1 or with the inhibitors combined. Both apoptosis and necroptosis activation contribute to cytotoxicity. d Western blots showing Tg-induced activation of the UPR by increased BiP/GRP78 and CHOP levels. Tg activated all three UPR branches to varying extents in a cell specific way as indicated by PERK phosphorylation (upper band) and ATF4 expression, enhanced expression of XBP1S and ATF6. Error bars indicate standard deviations. *p-value < 0.05

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