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. 2016 Feb 23;7(14):18050–18064. doi: 10.18632/oncotarget.7633

Figure 5. EF24 directly binds and inactivates TrxR1 in human gastric cancer cells.

Figure 5

A. TrxR1 enzyme activity was measured with/without EF24 treatment in vitro. B. Molecular docking of EF24 with TrxR1 protein was carried out with the docking software. C. The TrxR1 expression was determined by western blotting after knockdown with two different siRNAs for 48 h. D.-E. Knockdown of TrxR1 in SGC-7901 cells significantly increased the ROS levels D. and apoptotic cells E. induced by EF24. F. Dramatically augmentation of the EF24 cytotoxicity to gastric cancer cells by GSH depletion. G. EF24 and erastin in combination dramatically activated ER-stress pathway. H. NAC or catalase addition reversed combined treatment-induced expression of ER-stress related proteins. I. Blocking of ROS generation abolished the cytotoxicity of combined treatment.