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. 2012 Jan 18;14(3):266–277. doi: 10.1093/neuonc/nor226

Fig. 6.

Fig. 6.

Coupling lysosomal dysfunction with pan erbB inhibition leads to increased cytotoxicity. (A) Treatment with rapamycin (3 µM; 1 h pretreatment) did not affect chloroquine (CQ)–induced death (50 µM; 24–48 h) but (B) induced an increase in Akt activation. (C) Pretreatment with PD168393 (2 µM; 1 h pretreatment) triggered increased cytotoxicity in CQ-treated cells (36–72 h). * P < .05 relative to cells treated singly with CQ or PD168393. Immunoblot analyses demonstrated (D) an increase in levels of cleaved caspase-3 and (E) cleaved PARP in cells receiving dual treatment with CQ and PD168393 relative to cells treated with either agent alone (24 h). (F) Cells receiving dual treatment with BafA1 (100 nM) and PD168393 demonstrated increased cell death relative to cells receiving either agent alone (24 h). *P < .05 relative to cells treated singly with CQ or BafA1. (G) Cells receiving dual treatment with cytosine arabinoside (50 µM) or doxorubicin (0.5 µg/mL) and PD168393 did not demonstrate any difference in viability relative to cells receiving single treatment (24 h).