Fig. 6: Obatoclax disrupted tunicamycin-induced ER stress via lysosomal dysfunction and enhanced ER stress. | Cell Death Discovery

Fig. 6: Obatoclax disrupted tunicamycin-induced ER stress via lysosomal dysfunction and enhanced ER stress.

From: Inhibition of anti-apoptotic Bcl-2 family members promotes synergistic cell death with ER stress inducers by disrupting autophagy in glioblastoma

Fig. 6

A Immunofluorescence staining of Onda7 and DK-MG cell lines using Cyto-ID Green (autophagy detector) and Blue-white DPX (nuclear stain) under DAPI and FITC filters. Scale bar: 50 μm. B Autophagic flux was calculated as the intensity of fluorescence. Effects on autophagy are presented as fold change of fluorescence. The intensity of fluorescence in the DMSO control group was considered 0% (n = 3). **P < 0.01, ***P < 0.001, ****P < 0.0001. C LC3-II and p62 expression in the Onda7 cell line was detected via Western blotting after treatment with 1 µM obatoclax for 0, 4, 8, 16, 20, and 24 h. D LC3-II and p62 expression in the Onda7 cell line was detected via Western blotting 24 h after treatment with 1 µM obatoclax, 1 µM tunicamycin, or both. E PERK pathway-related expression in the Onda7 and DK-MG cell lines were detected via Western blotting 24 h after treatment with 50 µM Chloroquine, 1 µM tunicamycin, or both. F Fluorescence microscopy results of the flux in the mCherry-EGFP-LC3 plasmid-transfected DK-MG cell line. After transient transfection with mCherry-EGFP-LC3 plasmids, DK-MG cells were treated with the indicated treatment for 24 h. Scale bar: 100 μm. Concentrations: 1 µM obatoclax, 1 µM tunicamycin, 1 µM rapamycin, 50 µM chloroquine. G Quantitative data for yellow (mCherry-EGFP) or red (mCherry) dots in the cells counted (n = 4). Dots were detected using the Operetta CLSmachine. ****P < 0.0001.

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