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. 2018 Jul 13;14(10):1221–1231. doi: 10.7150/ijbs.25488

Figure 3.

Figure 3

AZD1775 and MLN0128 treatment suppressed downstream molecules, increased DNA damage, induced ER stress and apoptosis in SCLC cells. A. Suppressed PI3K/mTOR pathway activities in H69 and H82 cells upon treatment with AZD1775 (1000nM for H69, 250nM for H82), or MLN0128 (50nM), or combination of both, for 48 hours. Western blot of SCLC cell lysates with indicated antibodies; tubulin was used as loading control. B. Increased DNA damage and apoptosis in H69 and H82 cells upon treatment with AZD1775 (1000nM for H69, 250nM for H82), or MLN0128 (50nM), or combination of both, for 48 hours. Cell lysates were collected followed by western blot using indicated antibodies; tubulin was used as loading control. C. Induction of ER stress and activation of UPR and CHOP activation in H69 and H82 cells upon treatment with AZD1775 (1000nM for H69, 250nM for H82), or MLN0128 (50nM), or combination of both, for 24 hours. Cell lysates were collected followed by western blot using indicated antibodies; tubulin was used as loading control. D. Up-regulation of pro-apoptotic proteins in H69 and H82 cells upon treatment with AZD1775 (1000nM for H69, 250nM for H82), MLN0128 (50nM), or combination of both, for 48 hours. Western blot was performed with indicated antibodies; tubulin was used as loading control.