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Fig. 2 | Cancer Cell International

Fig. 2

From: RETRACTED ARTICLE: Excessive mitochondrial fragmentation triggered by erlotinib promotes pancreatic cancer PANC-1 cell apoptosis via activating the mROS-HtrA2/Omi pathways

Fig. 2

Erlotinib activates mitochondrial fragmentation in PANC-1 cells. a Mitochondrial fragmentation was determined using an immunofluorescence assay. Tom-20 was used to stain the mitochondria, and the average length of the mitochondria was calculated to quantify mitochondrial fragmentation. Mff antibody was used to lable the Mff, an mitochondrial fragmentation activator. FCCP and Mdivi-1 were used to activate or inhibit mitochondrial fragmentation, respectively. b Quantification of the mitochondrial length. c The relative Mff fluorescence intensity was evaluated in the presence of erlotinib treatment. FCCP and Mdivi-1 was used to activate or inhibit mitochondrial fragmentation, respectively. Mdivi-1, an antagonist of mitochondrial fragmentation, was added into the medium of erlotinib-treated cells. Meanwhile, FCCP, an agonist of mitochondrial fragmentation, was used to incubate with normal cells, which was used as the positive control group. dg The alterations of mitochondrial fission/fusion-related factors were measured using qPCR. Drp1 and Mff were pro-fission proteins, and their expressions were significantly increased in response to erlotinib treatment. In contrast, Mfn2 and Opa1 were pro-fusion factors, and their levels were downregulated by erlotinib application. h–j Western blotting for Mfn2 and Opa1 in response to erlotinib treatment. *p < 0.05

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