Neoplasms chemosensitization enhancing effects of nitric oxide donor compounds / 国际肿瘤学杂志

The chemosensitivity enhancive mechanism on nitric oxide includes three routes:adjust the expression level of hypoxia-inducible factor-1 α(HIF-1 α),classical nitric oxide signal pathway and combine with the reaction products of other molecules.Traditional nitric oxide donor compounds include nitroferricya-nide,organic nitrates,s-nitrosothiols,azo onium diol aldoxide,non-steroids anti-inflammatory drugs,whose function of antitumor and chemotherapy sensitization caused extensive attention.

Selective cyclooxygenase inhibitors increase paclitaxel sensitivity in taxane-resistant ovarian cancer by suppressing P-glycoprotein expression / 부인종양

OBJECTIVE: The purpose of this study was to investigate whether selective cyclooxygenase (COX) inhibitors promote paclitaxel-induced apoptosis in taxane-resistant ovarian cancer cells by suppressing MDR1/P-glycoprotein (P-gp) expression. METHODS: Taxane-resistant ovarian cancer cells were cultured with paclitaxel alone or combined with a selective COX inhibitors. The expression patterns of MDR1/P-gp and the ability of COX inhibitors to inhibit growth of taxane-resistant ovarian cancer cells were measured. The efficacy of prostaglandin E2 (PGE2) supplementation was measured to evaluate the mechanisms involved in suppressing MDR1 gene expression. RESULTS: P-gp was upregulated in taxane-resistant ovarian cancer cells compared to paired paclitaxel-sensitive ovarian cancer cells. An 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay showed that selective COX inhibitors significantly enhanced the cytotoxic effects of paclitaxel in taxane-resistant ovarian cancer cells via a prostaglandin-independent mechanism. These increased apoptotic effects were further verified by measuring an increased percentage of cells in sub-G1 stage using flow cytometry. Selective COX inhibitors suppressed MDR1 and P-gp expression. Moreover, combined treatment with paclitaxel and selective COX inhibitors increased poly (ADP-ribose) polymerase (PARP) cleavage in taxane-resistant ovarian cancer cells. CONCLUSION: Selective COX inhibitors significantly promote paclitaxel-induced cell death in taxane-resistant ovarian cancer cells in a prostaglandin-independent manner. COX inhibitors could be potent therapeutic tools to promote paclitaxel sensitization of taxane-resistant ovarian cancers by suppressing MDR1/P-gp, which is responsible for the efflux of chemotherapeutic agents.

Effects of neferine on gastric carcinoma apoptosis induced by vincristine / 中国药理学通报

AIM To study the effects of neferine on gastric car cinoma apoptosis induced by vincristine in vitro. METHODS Cytotoxicity assay was tested by MTT method. The influence of neferine to affect vincristine to induce gastric carcinoma apoptosis was detected by PI staining flow cytometry, AO/EB double fluorescence stain and terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL). RESULTS 2 5, 5,10 ?mol?L -1 neferine enhanced vincristine to inhibit the proliferation of SGC7901 cells; 10 ?mol?L -1 neferine enhanced vincristine (0 1, 0 5, 2, 4 mg?L -1 ) to induce SGC7901 cells apoptosis. CONCLUSIONS Neferine enhanced vincristine to induce gastric carcinoma cells apoptosis. It is inferred a kind of low poisonous and high effective chemosenstizers.

Synergistic effect of peroxiredoxin II antisense on cisplatin-induced cell death

Peroxiredoxin II (Prx II) is known not only to protect cells from oxidative damage caused by hydrogen peroxide (H2O2), but also to endow cancer cells with resistance to both H2O2 and cisplatin and to grant them radioresistance. In this study, we examined whether Prx II antisense could enhance cisplatin-induced cell death. When gastric cancer cells were transfected with various concentrations of Prx II antisense plasmid, pPrxII/AS, and then treated with the same concentrations of cisplatin, Prx II antisense enhanced cisplatin-induced cell death. The combination index (CI) at all doses of the combination was below 1, indicating that Prx II antisense sensitized cisplatin-induced cell death. This synergism was also observed in the cells transfected with a Prx II antisense oligomer. Our present results, therefore, suggest that Prx II antisense would be a very good sensitizer for cisplatin, and that Prx II as a target for chemosensitizers constitutes a promising avenue for future research.

Synergistic effect of peroxiredoxin II antisense on cisplatin-induced cell death

Peroxiredoxin II (Prx II) is known not only to protect cells from oxidative damage caused by hydrogen peroxide (H2O2), but also to endow cancer cells with resistance to both H2O2 and cisplatin and to grant them radioresistance. In this study, we examined whether Prx II antisense could enhance cisplatin-induced cell death. When gastric cancer cells were transfected with various concentrations of Prx II antisense plasmid, pPrxII/AS, and then treated with the same concentrations of cisplatin, Prx II antisense enhanced cisplatin-induced cell death. The combination index (CI) at all doses of the combination was below 1, indicating that Prx II antisense sensitized cisplatin-induced cell death. This synergism was also observed in the cells transfected with a Prx II antisense oligomer. Our present results, therefore, suggest that Prx II antisense would be a very good sensitizer for cisplatin, and that Prx II as a target for chemosensitizers constitutes a promising avenue for future research.

Effect of CM on Interventional Therapy on Middle and Late Stage Malignant Tumors / 实用放射学杂志

Objective To determine the clinical use of CM on interventional therapy for middle and late stage cancer.Methods We observed the effect of clinical administration on the patients with interventional therapy or inteventional therapy plus CM,control with themselvies.Results 38(76%) out of 50 patients got better than that of preadministration,cancer mass decreased.Conclusion CM can increase the sensitivity of carcinoma cells to chemicals and decrease its sideeffect.