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. Author manuscript; available in PMC: 2013 Dec 1.
Published in final edited form as: Mol Cancer Res. 2012 Oct 10;10(12):1567–1579. doi: 10.1158/1541-7786.MCR-12-0209-T

Figure 3. Multimodality treatment-induced ROS production, JNK activation, and Bcl-xL phosphorylation in CX-1 cells.

Figure 3

(A) Cells were treated with/without 10 mM NAC for 30 min followed by oxaliplatin/Mapa/hyperthermia and incubated with CMH2DCFDA (25 µM). Morphological features and fluorescent signals were detected with a phase-contrast microscope and a fluorescence microscope, respectively. (B) Cells were treated with oxaliplatin/Mapa/hyperthermia and immunoblotted with anti-phospho-JNK or anti-JNK antibodies. (C) Cells were pretreated with 10 mM NAC for 30 min followed by oxaliplatin/Mapa/hyperthermia. PARP cleavage, phospho-JNK and JNK were detected. (D) Cells were treated with oxaliplatin/Mapa/hyperthermia and immunoblotted with anti-phospho-Bcl-xL or anti-Bcl-xL antibody. (E) Cells were pretreated with JNK-1 inhibitor SP600125 followed by oxaliplatin/Mapa/hyperthermia and immunoblotted with anti-PARP, anti-phospho-Bcl-xL and anti-Bcl-xL antibody. (F) Transfectants with control plasmid (pcDNA), wild-type Bcl-xL (Bcl-xL-WT), Ser62/Ala phospho-defective Bcl-xL mutant (Bcl-xL-S62A), or Ser62/Asp phospho-mimic Bcl-xL mutant (Bcl-xL-S62D) were treated with oxaliplatin/Mapa/hyperthermia and immunoblotted with anti-PARP or anti-Bcl-xL antibody. Actin was used to confirm the equal amount of proteins loaded in each lane.