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. 2016 Jun 17;7(32):51854–51864. doi: 10.18632/oncotarget.10126

Figure 4. The PERK inhibitor induced tunicamycin-mediated apoptosis in cancer stem-like cells.

Figure 4

Sphere-forming cells were untreated (control) or treated with 0.03 μM tunicamycin (TM) and/or 1.5 μM GSK 2606414 (a PERK inhibitor: PERKi), or 7 μM 4μ8C (an IRE1α inhibitor: IRE1i) for 72 hours. A. After the treatment, cells were subjected to PI/Annexin-V staining and analyzed by flow cytometry. B. A quantitative analysis of PI-negative/Annexin-V-positive apoptotic cells showed that the proportion of apoptotic cells in sphere-forming cells was clearly increased by the PERKi combined with tunicamycin treatment. The values shown represent the means ± SEM (*p < 0.05). C. After being treated, cells were fixed and stained with propidium iodide for a flow cytometry assay. A quantitative analysis of sub-G1 region (M1) cells showed that the tunicamycin+PERK inhibitor treatment induced apoptosis in sphere-forming cells. The values shown represent the means ± SEM (*p < 0.05).