| The incidence of prostate adenocarcinoma has increased in recent years. Although most patients respond initially to androgen-ablative therapies, the prostate adenocarcinoma cells eventually and inevitably lose their sensitivity to an-drogen. Presently available treatments for advanced, hormone-resistant prostate aadenocarcinoma are only marginally effective. Therefore, there is increasing urgency to develop new and effective strategies to prevent and treat prostate ade-nocinoma.Epidemiological, clinical, animal and laboratory studies have all provided evidence for prostaglandins and other eicosanoids in the tumorigenesis and growth. Cyclooxygenase(COX) , also referred to as prostaglandin endoperoxide synthase, is the key enzyme in the conversion of arachidonic acid( AA) to prostaglandins and other eicosanoids. Two isoforms of COX have been identified, namely COX-1 and COX-2. COX-1 is the constitutive gene, whereas COX-2 is inducible gene. Cytokines, growth factors, oncogenes, and tumor promoters have been found to induce COX-2 up-expression in order to produce prostaglandins ( PGs) for various inflammatory stimulation. Recent years studies have been founded that COX-2 played a key role in driving tumourigenesis and growth. PGE2, a major COX-2 derived product, has been reported to stimulate the tumor cell growth and inhibit the apoptosis. There are considerable reasons to believe that it could be reduced the production of PGs through inhibiting COX in order to inhibit the tumor cell proliferation and promote the apoptosis. Therefore, it is important to reduce the production of the PGs in prevention, treatment and prognosis. Nonsteroid anti -inflammatory drugs(NSAIDs) are COX inhibitors, which can be divided into three categories based on the difference of inhibition role inCOX: (1)COX-1 selective inhibitors, (2) COX-2 selective inhibitors, (3)COX non-selective inhibitors. Studies have showed that the potential of the NSAIDs for antiadenocinoma although the precise mechanisms for the antiadenocinoma effects of NSAIDs are unknown , but the ability of these drugs to induce cell cycle arrest and apoptosis, to inhibit the angiogenesis, tumor infiltration and metastasis has received much attention in recent years.NS398 is a NSAID that is highly selective inhibitor for COX-2, it can inhibit the carcinogensis and growth through inhibiting COX-2 with lower side effects, therefore it maybe have potential in chemical prevention for prostate ad-enocinoma. To investigate if NS398 can inhibit the proliferation of the human prostate carcinoma cells and promote the tumor cell apoptosis and to study the possible mechanisms and provide experimental data for the prevention and treatment of prostate adenocinoma, we observed the effect of NS398 on human prostate adenocinoma cell line, PC-3, in vitro.Methods1. RT-PCR assay: RT-PCR assay was employed to observe the expression of C0X-2mRNA before or after NS398 treatment.2. MTT assay: To observe the proliferation of PC-3 cell under the treatment with NS398.3. FCM Assay for analysis of cell cycle.4. DNA Ladder electrophoresis for Apoptotic Cells.5. Transmission electron microscope for Apoptotic Cells.6. Western-blot assay for expression change of COX-2 cyclinD cyclinE bcl-1 bax erk erk-p before and after treatment with NS398.7. Radioimmunoassay for PGE2 measurement.8. Statistical Methods.Statistical analysis was performed using SPSS for windows 10. 0 software. The results of human prostate adenocarcinoma cell line PC-3 treated with NS398 was expressed as mean 土 s. And comparisons of means were carried out by one way ANOVA-Dunnett t test; difference with a value of p <0.05 were consideredstatistically significant.Results1. The human prostate adenocarcinoma cell line , PC-3, express COX -2 protein and COX -2 mRNA. With the increasing of concentration of NS398, the expression level of COX -2 protein and COX -2 mRNA decreased.2. The results of MTT assay indicated that NS398 induced significant growth inhibition...
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