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. 2021 Apr 8;11:671180. doi: 10.3389/fonc.2021.671180

Figure 2.

Figure 2

CPT-induced autophagy was a survival signal in esophageal cancer cells. (A, B) The proliferation inhibition by CPT treatment was significantly increased by simultaneously blocking autophagy with siBeclin1 or siATG5. The combination of siBeclin1 or siATG5 with CPT in EC1 and EC109 cells significantly increased proliferation inhibition by ATPLite assay (n = 3). (C, D) Blocking of autophagy pathway by Beclin1 or ATG5 siRNA silencing amplified CPT-induced apoptosis. The combination of siBeclin1 or siATG5 with CPT in EC1 and EC109 cells significantly increased apoptosis by Annexin V-FITC/PI double-staining analysis (n = 3). (E, F) Beclin1 or ATG5 knockdown increased cleaved PARP expression induced by CPT. Cells were transferred with siRNAs against Beclin 1 (E) or ATG5 (F) for 48 h, and then treated with CPT at 2.5 μmol/L for 24 h. Knockdown efficiency and cleaved PARP were assessed by IB analysis. Data were presented as mean ± S.E.M. ***P < 0.001.