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ObjectiveTo investigate the effects of glioma microenvironment and COX-2 inhibitor celecoxib on the phenotypes and function of dendritic cell (DC).MethodsThe expression of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) production were detected in glioma C6 cells treated with different concentration of celecoxib.Monocytes were isolated from human peripheral blood and cultured with 200 ng/ml rhGM-CSF and 50 ng/ml rhIL-4,either C6 tumor cells supernatant (TSN) or TSN from C6 cells treated with celecoxib to generate DCs.Cell morphology was observed.Cell phenotype including CD1a,CD80,CD83 and D86 were analyzed on a FACScan.Production of IL-12 in DC supernatant and the potential to stmiulate allogeneic T cell proliferation were detected.ResultsThe expression of COX-2 and PGE2 production in C6 cells decreased after treated with celecoxib in a concentration dependant manner.Typical DCs were induced in all groups and the expression of CD1a ((75.56±2.40)％,(75.09±3.67)％,(76.03 ±3.43)％),CD83((72.04±3.45)％,(71.44±3.78)％,( 73.63 ± 3.31 ) ％ ) had no difference (P ＞ 0.05 ).Expression of CD80 ( ( 58.41 ± 3.85 ) ％ ),CD86 ( ( 58.22 ±3.25)％ ) in DC with TSN obviously decreased compared with normal group( (70.36 ± 2.91 )％,(69.31 ±4.29 ) ％,P ＜ 0.01 ) as well as the IL-12 production ( ( 137.88 ± 5.33 ) pg/ml,( 186.04 ± 4.76 ) pg/ml) and the potential to stmiulate allogeneic T cell proliferation ( P ＜ 0.01 ).Celecoxib increased the expression of CD80,CD86 (66.83 ± 2.51,63.51 ± 5.47,P＜ 0.01 ) in DC and the same as IL-12 production( ( 170.31 ± 3.46) pg/ml,P ＜ 0.01 ) and the potential to stmiulate allogeneic T cell proliferation ( P ＜ 0.01 ),which were lower than the normal level.ConclusionGlioma microenvironment may induce the celecoxib can inhibit the expression of COX-2 and PGE2 in gliomas cells and improve the phenotypes and function defect of DCs.
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Objective To investigate the expression of cyclooxygenase-2 (COX-2) and epidermal growth factor receptor (EGFR) in astrecytomas, as well as the correlation between them. Methods The expression of COX-2, EGFR and PCNA were respectively detected by immunohistochmical (S-P) method in 68 astrocytomas and 5 cases normal brain tissue. Proliferation index (PI) was calculated and the correlation of COX-2, EGFR and PI was analyzed. Results COX-2 and EGFR were negative expression in normal brain tissue. The positive expression rate of COX-2 and EGFR in high grade astrocytomas was significantly higher than that in low grade astrocytomas(73.53% vs 44. 18% ,67.65% vs 38.24%, P <0. 01 ), and the PI was significantly higher than that in low grade astrocytumas as well as normal brain tissue(46.11 ± 10. 68vs 23. 04±6. 25,4. 52±0. 95, P <0. 01 ). The PI in COX-2 positive group was higher than that in negative group( P <0. 01 ). The positive expression rate of COX-2 in the group with EGFR positive expression was higher than that in the negative group. Conclusions The expression of COX-2 and EGFR was related to pathological feature of astrocytomas. COX-2 may promote the proliferation of tumor cells. There was a static correlation between the expression of EGFR and COX-2 in astrocytomas. EGFR signal transduction probably modulated the expression of COX-2 in astrocytomas cells.