In conclusion, despite the potential importance of inflammation in prostate carcinogenesis, results from our large study of five PTGS2 SNPs does not support a strong association between PTGS2 variants and prostate cancer risk in non-Hispanic white men.
The purpose of this case-control study was to evaluate the association between prostate cancer risk and 14 such SNPs in the PTGS2, PTGES2, ALOX5, ALOX5AP, and LTA4H genes.
Two common polymorphisms in the prostaglandin-endoperoxide synthase 2 (PTGS2) gene, rs20417 and rs689470, have been found to alter the risk for prostate cancer, but the various studies are not in agreement.
The importance of HIF-1alpha in tumor progression makes it a logical target for chemoprevention strategies in patients at higher genetic risk of breast and prostate cancer with Cox 2 inhibitors or 2-methoxyestradiol, as well as a target for new approaches to inhibiting angiogenesis.
In conclusion, NFKB1 -94 ins/del and COX-2 (-1195G>A) polymorphisms may be, respectively, associated with decreased and increased prostate cancer risk in the Chinese population.
These findings in conjunction with findings in other populations of African descent might suggest a common causal variant for prostate cancer in COX-2, or a variant in a nearby gene.
All-NSAIDs use was inversely associated with prostate cancer: OR 0.77, 95% CI 0.61-0.98, especially in men using NSAIDs that preferentially inhibit COX-2 activity (OR 0.48, 95% CI 0.28-0.79).
These findings provide evidence that the G allele of COX2 promoter G-765C may be associated with the development of prostate cancer and may be a useful marker for early detection of prostate cancer.
This meta-analysis suggested that the functional COX2 -765G>C polymorphism, located in the COX2 gene promoter, is unlikely to be associated with PC risk.
The variant genotype CC of COX-2 +8473 T>C polymorphism was found to be significantly associated with the overall higher risk of PCa (p = 0.045; OR = 1.82).
To elucidate the effects of COX-2 on p53 in response to hypoxia, we transfected the COX-2 gene into the p53-positive, COX-2-negative MDA-PCa-2b human prostate cancer cell line.
The expression of Ki-67, PSCA, and Cox-2 biomarkers along with other clinicopathologic factors were prognostic factors for BCR in patients with clinically localized prostate cancer following radical prostatectomy.
Thus, the potential therapeutic role of curcumin and selective COX-2 inhibitors in combination with available VIP antagonists should be considered in prostate cancer therapy as supported by their inhibitory activities on tumor cell growth.