CB13 a novel PPARγ ligand overcomes radio-resistance via ROS generation and ER stress in human non-small cell lung cancer

摘要

a The chemical structures and molecular formulas of CB13 and Cig. b 3T3-L1 cells were transiently transfected with 2 μg of the PPAR response element reporter gene (pGL3-PPRE vector) and the pGL3-PPRE vector and treated with CB13 or Cig at the indicated doses (CB13, 10 and 30 μΜ; Cig, 10 μΜ); *P < 0.05. c CB13-mediated (30 μΜ, 24 h), Cig-mediated (10 μΜ, 24 h), or CB13/GW9662-mediated adipocyte differentiation was assessed by the presence of Oil Red O-stained droplets. Oil Red O-stained cells were detected using a light microscope and scoring cells from each dish at ×400 magnification. d Oil Red O quantification was performed by adding a dye extraction solution to each well and measuring the absorbance at 510 nm. Values indicate the means ± SE of three replicates (*P < 0.05, **P < 0.01 vs. control; Student’s t-test). e Effect of GW9662 on CB13-treated 3T3-L1 cells. 3T3-L1 cells were pretreated with GW9662 (20 μΜ) for 4 h and then treated with CB13 (30 μΜ). 3T3-L1 cells were also treated with Cig (10 μΜ) as a control. Total lysates were interrogated by Western blot analysis to confirm inhibition of PPARɣ. β-actin was used as a protein loading control.