Effect of PPAR-γ on proliferation of human pancreatic cancer BxPc-3 cells

Objective To evaluate the effect of promoting the expression of peroxisome proliferator-activated receptor-γ （PPAR-γ） on the proliferation of human pancreatic cancer BxPc-3 cells. Methods BxPc-3 cells were cultured and pretreated with PPAR-γ agonist rosiglitazone with a final concentration of 5, 10, 20 and 40 μmol/L, respectively. Western blot was used to detect the expression of PPAR-γ protein. MMT assay was employed to observe the cell proliferation. Results There was no statistical significance in the PPAR-γ expression levels between BxPc-3 cells treated with 5 and 10 μmol/L rosiglitazone and control cells （both P > 0.05）. The expression levels of PPAR-γ were gradually up-regulated after treatment with 20 and 40 μmol/L rosiglitazone, which had statistical significance compared with that in the control group （both P < 0.05）. The expression level of PPAR-γ in the 40 μmol/L rosiglitazone group was significantly higher than that in the 20 μmol/L rosiglitazone group （P < 0.05）. The proliferative activity of BxPc-3 cells treated with 5 and 10 μmol/L rosiglitazone was 0.60±0.07 and 0.57±0.06, which had no statistical significance compared with that in the control group （both P > 0.05）. The proliferative activity of BxPc-3 cells treated with 40 μmol/L rosiglitazone was 0.30±0.02, significantly lower than those in the 20 μmol/L rosiglitazone group （0.45±0.03）, control group, 5 and 10 μmol/L rosiglitazone groups （all P < 0.05）. Conclusion Promoting PPAR-γ expression can effectively inhibit the proliferation of human pancreatic cancer BXPC-3 cells.