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Fig. 3 | Cancer Cell International

Fig. 3

From: RETRACTED ARTICLE: Excessive mitochondrial fragmentation triggered by erlotinib promotes pancreatic cancer PANC-1 cell apoptosis via activating the mROS-HtrA2/Omi pathways

Fig. 3

Mitochondrial fragmentation promotes mitochondrial ROS (mROS) overproduction. a The levels of mROS was measured using a mitochondrial ROS probe, and a quantitative analysis of mROS was conducted using flow cytometry. b Quantification of mROS in PANC-1 cells treated with erlotinib. The antagonist Mdivi-1 was added to the medium of PANC-1 cells to inhibit the activity of mitochondrial fragmentation. cf An ELISA was used to evaluate the concentrations of factors involved in the cellular redox status. Mn-SOD, GSH and GPX are antioxidant factors whereas MDA is an end product of cellular membrane oxidation, was detected using an ELISA kit. g PANC-1 cells were treated with erlotinib or Mdivi-1, and then cellular total ATP production was measured using an ELISA. hk Mitochondrial respiratory complex expression was determined by western blotting in the presence of erlotinib. *p < 0.05

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