| Objective:To investigate the expression of PPAR-γ(peroxisome proliferator–actived receptorγ) and 15-LOX-2(15-lipoxygenase-2) in tissue of prostate cancer and BPH, and evaluate their possible significances.Methods: Immunohistochemistry was used to detect the expression of PPAR-γand 15-LOX-2 in 28 cases of prostate cancer and 26 cases of BPH by control.Results:The positive rate of PPAR-γin prostate cancer and BPH were 64.29%(18/28) and 26.92%(7/26) respectively. The expression of PPAR-γprotein in prostate cancer and BPH was statistically significant (χ~2=4.84,P<0.05). The positive rate of 15-LOX-2 in prostate cancer and BPH were 17.86%(5/28)and 76.92%(20/26) respectively. There was significant difference(χ~2=9.00,P<0.05) observed between the expression of 15-LOX-2 in prostate cancer and BPH. There was a significant difference between the PPAR-γexpression of T2 stage and T3 stage(H=4.103,P<0.05),but there was no significant difference between the 15-LOX-2 expression of T2 stage and T3 stage(H=0.076,P>0.05). The expression of PPAR-γin prostate cancer with Gleason≥7 was significantly higher than with Gleason<7(H=5.306,P<0.05), but there was no significant difference between on 15-LOX-2 expression between with Gleason≥7 and with Gleason<7(H=0.313,P>0.05).Conclusion: The expression of PPAR-γprotein increased in prostate cancer and was related with pathologic stage and Gleason; the expression of 15-LOX-2 decreased in prostate cancer. They may be molicular markers in prostate cancer. Objective:To explore the expression of PPAR-γ(peroxisome proliferator-activated receptorγ) in prostate carcinoma and to investigate the inhibitory effects and mechanisms of Telmisartan, a PPAR-γpartly agonist on human prostate carcinoma cell line PC3.Methods:The expression of PPAR-γin PC3 cells was determined using Westernblot and RT-PCR.Cells cultured in vitro were treated with Telmisartan for intervention. MTT assay, Immunofluorescence staining were used to detect the effects on the growth, apoptosis of the human tumor PC3 cells respectively.Results:Western blot and RT-PCR detection showed there were PPAR-γexpressed in PC3 cells. MTT assay showed that there were different degrees of Proliferation on PC3 cells except which were not interfered with Telmisartan.There was no significant difference on the inhibition of cell proliferation between treated with the same concentration of Telmisartan(0μmol/L,25μmol/L,50μmol/L,100μmol/L)whether mixed in PPAR inhibitor GW9662 or not(F=8.336,P>0.05); There was significantly different on the inhibition of cell proliferation between treated with different concentration of Telmisartan whether mixed in GW9662 or not(group I: F=18.372,P<0.05,group II :F=25.561,P<0.05); Treated with Telmisartan alone 100μmol / L for 24h, 48h and 72h , the average cell survival rate was significantly decreased. The average cell survival rate of 24h, 48h and 72h was 29.22%, 23.00% and 21.29% respectively. cells survival rate of 24h and 48h was significantly different(χ~2=1.003, P <0.05); cells survival difference of 48h and 72h was also statistically significant (χ~2=8.480,P<0.05).The results of fImmunofluorescence staining suggested that Telmisartan could induce PC3 cells early apoptosis.Conclusion:Telmisartan could induce PC3 cells early apoptosis and decrease cell survival rate. This may be a new treatment of hormone-refractory human prostate cancer . |
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