Daurisoline Inhibits ESCC by Inducing G1 Cell Cycle Arrest and Activating ER Stress to Trigger Noxa-Dependent Intrinsic and CHOP-DR5-Dependent Extrinsic Apoptosis via p-eIF2<i>α</i>-ATF4 Axis

<div>ATF4 was responsible for daurisoline-induced intrinsic and extrinsic apoptosis. (a) EC1 and ECA109 cells were treated with DAS as described above and were subjected to western blot. (b) The mRNA level of ATF4 was quantified by Q-PCR. (c-e) EC1 and ECA109 cells were transfected with control or two siRNA sequences of ATF4, then treated with DAS (30 <i>μ</i>M) for 24 hours. Apoptosis induction was quantified by Annexin V-FITC/PI double-staining and FACS analysis. Proteins were extracted and detected by western blot. The mRNA level of ATF4, CHOP, DR5, and Noxa was quantified by Q-PCR.</div>

Oxidative Medicine and Cellular Longevity

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Figure 6

Figure 6: Daurisoline Inhibits ESCC by Inducing G1 Cell Cycle Arrest and Activating ER Stress to Trigger Noxa-Dependent Intrinsic and CHOP-DR5-Dependent Extrinsic Apoptosis via p-eIF2<i>α</i>-ATF4 Axis 

Figure 6 | Daurisoline Inhibits ESCC by Inducing G1 Cell Cycle Arrest and Activating ER Stress to Trigger Noxa-Dependent Intrinsic and CHOP-DR5-Dependent Extrinsic Apoptosis via p-eIF2α-ATF4 Axis 