Objective：The role of methylseleninic acid （MSeA）, a selenium compound, has been documented in cancer chemoprevention. However, the therapeutic effect of MSeA in combination with paclitaxel, a chemotherapeutic agen...Objective：The role of methylseleninic acid （MSeA）, a selenium compound, has been documented in cancer chemoprevention. However, the therapeutic effect of MSeA in combination with paclitaxel, a chemotherapeutic agent used to treat ovarian cancer, is unknown. In this study, we investigated the effect of combination treatment of MSeA and paclitaxel against ovarian cancer cells. Methods：Ovarian cancer cells（A2780） were treated with different concentrations of MSeA, paclitaxel alone or in combination. The individual and combined concentrations of drugs that achieved certain cells growth/death were determined using a sulforhodamine B（SRB） assay. Drug effects on cell viability were further confirmed using floating cell count and trypan blue exclusion assay. The mean Values ± standard deviation were calculated and compared between treatment groups using unpaired t test. Results： The concentration of paclitaxel alone that inhibited 50% of cell growth（IC50） was 0.5 μmol/L. This concentration increased to 1.2 μmol/L when paclitaxel was given in sequential combination with MSeA. The number of dead cells after the combination treatment did not show a significance increase when compared with drug alone. Conclusion：Pretreatment with MSeA did not enhance the paclitaxel effect against A2780 ovarian cancer cells.展开更多
基金supported in part by a research grant form the American Cancer Society(IRG0219706)a comprehensive cancer center support grant from the National Cancer Institute(CA016056)
文摘Objective：The role of methylseleninic acid （MSeA）, a selenium compound, has been documented in cancer chemoprevention. However, the therapeutic effect of MSeA in combination with paclitaxel, a chemotherapeutic agent used to treat ovarian cancer, is unknown. In this study, we investigated the effect of combination treatment of MSeA and paclitaxel against ovarian cancer cells. Methods：Ovarian cancer cells（A2780） were treated with different concentrations of MSeA, paclitaxel alone or in combination. The individual and combined concentrations of drugs that achieved certain cells growth/death were determined using a sulforhodamine B（SRB） assay. Drug effects on cell viability were further confirmed using floating cell count and trypan blue exclusion assay. The mean Values ± standard deviation were calculated and compared between treatment groups using unpaired t test. Results： The concentration of paclitaxel alone that inhibited 50% of cell growth（IC50） was 0.5 μmol/L. This concentration increased to 1.2 μmol/L when paclitaxel was given in sequential combination with MSeA. The number of dead cells after the combination treatment did not show a significance increase when compared with drug alone. Conclusion：Pretreatment with MSeA did not enhance the paclitaxel effect against A2780 ovarian cancer cells.
