Pristimerin Exacerbates Cellular Injury in Conditionally Reprogrammed Patient-Derived Lung Adenocarcinoma Cells by Aggravating Mitochondrial Impairment and Endoplasmic Reticulum Stress through EphB4/CDC42/N-WASP Signaling
PRIS induces mitochondrial dysfunction via ER stress responses in CRLCs. Cells were treated with 2, 4, 8, and 16 μM PRIS for 24 h. (a) ROS generation was determined by the amount of cellular DCF formation (). (b) After treatment, cells were incubated with 20 nM DiOC6 for 30 min and MMP was measured by flow cytometry (). (d, e) CRLCs were pretreated with 5 mM NAC for 60 min, then incubated with 4 or 8 μM PRIS for 24 h; ROS generation was determined by the amount of cellular DCF formation (), and GSH/GSSG was measured and the ratio was calculated (). (f, g) Cells were treated as described above in (d, e), then assessed for MMP by flow cytometry (). Cell viability was determined by MTS assay (). (h) CRLCs were pretreated with 5 mM NAC for 60 min, then incubated with 4 μM PRIS for 24 h, and indicated protein expressions were measured by Western blot. (i–k) Cells were transfected with scrambled (Scr) siRNA or CHOP siRNA for 48 h and then treated with 4 μM PRIS for 24 h, and indicated protein expression was detected by Western blot. All Western blot band intensities were normalized to GAPDH. Data are presented as ,,.
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