PPAR Enhances Cancer Cell Chemotherapy Sensitivity by Autophagy Induction

Figure 7

PPAR/autophagy enhances chemotherapy sensitivity to cancer cells. (a) SW480 cells were transfected with vector or PPARα plasmids for 36 h. After that, cells were treated with camptothecin (60μM), taxol (300μM), etoposide (600μM), and cisplatinum (30μM) for 6 h. Cell lysates were subjected to Western blot. (b) SW480 cells were transfected with ctrl shRNA or PPARα shRNA plasmids for 36 h. After that, cells were treated with camptothecin (60μM), taxol (300μM), etoposide (600μM), and cisplatinum (30μM) for 6 h. Cell lysates were subjected to Western blot. (c) SW480 cells were transfected with ctrl shRNA or PPARα shRNA plasmids for 36 h. After that, cells were treated 100μM cisplatin or 100μM cisplatin +10μm clofibrate for 12 h. Cell lysates were subjected to Western blot. SW480 cells were injected subcutaneously in nude mice. After two weeks, mice were treated without or with cisplatin (3mg/kg), Clo (20mg/kg/day), or Clo (20mg/kg/day) +cisplatin (3mg/kg) for another two weeks by intraperitoneal injection. Tumor volume (d) or weight (e) was measured. Results are expressed as means ± SEM (n=5). P<0.05, P<0.01. (f) Tumor lysates were subjected to Western blot. (g) The model of PPARα/Bcl2/autophagy signaling inhibits tumor growth and chemotherapy sensitivity. Data are triplicates from three independent experiments.

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