Objective To investigate the effects of staphylococcus aureus (S.aureus) DNA on anti-tumor in vivo and its mechanism. Methods The chromatic DNA purified from S.aureus was used in the experiments of antitumor in vivo, and immunological indices were measured. Results S.aureus DNA could inhibit the tumor growth by peritoneal injection, increase the serum IFN-? level and regulate the serum TNF-? level in the nude mice carrying transplant tumor. Conclusion S aureus DNA has a characteristic of anti-tumor immunity, and can be used in immunotherapeutic treatment of tumors.

BACKGROUNDTo investigate the expression of COX-2 and its relation to clinical pathophysiological features and prognosis in non-small cell lung cancer (NSCLC).

METHODSThe expression of COX-2 protein was detected in 52 NSCLC tissues by immunohistochemical (S-P) method.

RESULTSThe positive COX-2 expression was observed in 25 (48.1%) cases of NSCLC tissues. The positive rate of COX-2 expression was 76.5% and 34.3% in adenocarcinoma and squamous cell carcinoma respectively (P < 0.01). The positive rate of COX-2 expression in T3+T4 disease (92.3%) was remarkably higher than that in stage T1+T2 (33.3%) (P < 0.01). There was a remarkable difference in COX-2 expression rate between clinical stage I+II (28.1%) and clinical stage III+IV (80.0%) groups (P < 0.01). The positive rate of COX-2 expression was 83.3% in those with lymph node metastasis, but only 17.9% in those without lymph node metastasis (P < 0.01). In addition, there were significant differences in positive rate of COX-2 expression among patients with ≤2, > 2 but < 5, ≥5 years of survival span respectively (P < 0.01).

CONCLUSIONSOverexpression of COX-2 in NSCLC, especially in adenocarcinoma, is closely related to invasion, lymph node metastasis and clinical stage of lung cancer. It may play a role in development of NSCLC, and also may be a prognostic marker.

BACKGROUNDIn recent years, many investigations have showed that COX-2 inhibitors not only inhibit the growth of tumor cells but also enhance the cytotoxicity of anticancer drugs, such as NS-398, a selective COX-2 inhibitor. But the effect of NS-398 combined with chemotherapy agent cisplatin on growth of lung adenocarcinoma cells and its mechanism are still unknown. The aim of this study is to investigate the effect of NS-398 combined with cisplatin on proliferation of human lung adenocarcinoma cell lines, and to explore their mechanisms.

METHODSSynergistic effect of NS-398 and cisplatin on proliferation of human lung adenocarcinoma cell lines was detected by MTT growth assay, and data were analyzed by SPSS general linear models procedure to determine the IC₅₀ of each drug alone. Combined index (CI) was analyzed to determine the combined effect of drugs. Apoptosis and cell cycle distribution were detected by fluorescence staining of Acridine orange (AO) and Ethidium bromide (EB) and flow cytometry.

RESULTSThe various concentration of NS-398 in combination with cisplatin resulted in the reduction of IC₅₀ of cisplatin by 48.25%-62.44% in A549 cells, and by 43.34%-69.61% in SPC-A-1 cells. The CI of NS-398 and cisplatin in the two cell lines ranged from 0.4 to 0.9, which indicated that they acted in slight synergistic to synergistic pattern. The apoptotic rate at 24h and 48h in the combined groups was significantly higher than those of the control groups, and the S-phase cell fractions at 48h and 72h were obviously higher than those of the control groups. There was a positive correlation between apoptotic rate and S-phase cell fraction in the combined groups (r=0.882,P= 0.01).

CONCLUSIONSNS-398 can improve growth inhibition of cisplatin on lung adenocarcinoma cells, and the two agents act in synergistic way. This synergistic effect may be related to apoptosis pathway.

BACKGROUNDRecent studies have shown that NS-398, a highly selective COX-2 inhibitor, can enhance the inhibition effects of cisplatin on adenocarcinoma cell proliferation, but the mechanism is still unknown. The aim of this study is to explore the mechanism about the synergistic effects of NS-398 and cisplatin to human lung adenocarcinoma cell line.

METHODSDifferentially expressed proteins were separated in human lung adenocarcinoma cells treated with NS-398 and/or cisplatin by immobilized pH gradient-based two-dimensional gel electrophoresis (2-DE), then 19 out of obtained proteins were identified by peptide mass fingerprint (PMF) based on matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS) and database searching.

RESULTSThere were 22 down-regulated proteins and 2 up-regulated proteins in NS-398+cisplatin combination group compared with control groups. Finally six proteins were identified, in which some were cytokeratins, some were associated with proliferation and apoptosis, and the others were involved in metabolism of tumor cells.

CONCLUSIONSThe down-regulation of HSP90 and triosephosphate isomerase may be related to the synergistic effects of NS-398 and cisplatin on human lung adenocarcinoma cells.