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目的探讨盐霉素对前列腺癌DU145干细胞的影响及其可能的机制,为盐霉素的临床应用提供理论依据。方法盐霉素处理DU145细胞,以ALDH为肿瘤干细胞标记物,用流式细胞仪检测处理后ALDH阳性的DU145干细胞的百分比。盐霉素处理DU145细胞后,用Western Blot法检测mTOR信号通路相关蛋白m-TOR、p-70s6k、p-p70s6、p-s6等的表达变化。盐霉素结合mTOR信号通路抑制剂雷帕霉素处理DU145细胞,利用流式细仪检测ALDH阳性的DU145干细胞百分比。结果盐霉素显著性抑制ALDH阳性的DU145干细胞(抑制率为77.78%),是紫杉醇的2倍(抑制率为38.64%)。盐霉素抑制mTOR信号通路相关分子m-TOR、p-70s6k、p-p70s6、p-s6等蛋白的表达,具有时间依赖性和剂量依赖性。盐霉素结合雷帕霉素能够抑制ALDH阳性的DU145干细胞比例(抑制率为77.95%)。结论盐霉素可能通过抑制mTOR通路信号来发挥抑制肿瘤干细胞的作用。
Objective To explore the effect of salinomycin on prostate cancer DU145 stem cells and its possible mechanism, and to provide a theoretical basis for the clinical application of salinomycin. Methods Salinomycin-treated DU145 cells were treated with ALDH as tumor stem cell marker. The percentage of ALDH-positive DU145 stem cells treated by salinomycin was detected by flow cytometry. Salinomycin treated DU145 cells, the expression of mTOR signaling pathway associated protein m-TOR, p-70s6k, p-p70s6, p-s6 and other changes were detected by Western Blot. Salinomycin combined with mTOR inhibitor rapamycin treatment of DU145 cells, the use of flow cytometer ALDH-positive DU145 stem cell percentage. Results Salinomycin significantly inhibited ALDH-positive DU145 stem cells (77.78% inhibition rate), which was twice as high as that of paclitaxel (inhibition rate was 38.64%). Salinomycin inhibited the expression of mTOR signaling pathway related molecules m-TOR, p-70s6k, p-p70s6, p-s6 and other proteins in a time-dependent and dose-dependent manner. Salinomycin combined with rapamycin can inhibit ALDH-positive DU145 stem cell ratio (77.95% inhibition rate). Conclusion Salinomycin may inhibit cancer stem cells by inhibiting the signal of mTOR pathway.