首页> 美国卫生研究院文献>Acta Pharmacologica Sinica >Acetyl-11-keto-β-boswellic acid suppresses docetaxel-resistant prostate cancer cells in vitro and in vivo by blocking Akt and Stat3 signaling thus suppressing chemoresistant stem cell-like properties
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Acetyl-11-keto-β-boswellic acid suppresses docetaxel-resistant prostate cancer cells in vitro and in vivo by blocking Akt and Stat3 signaling thus suppressing chemoresistant stem cell-like properties

机译:乙酰基-11-酮基-β-乳香酸可通过阻断Akt和Stat3信号传导在体内外抑制多西他赛耐药的前列腺癌细胞从而抑制类化学药品的干细胞特性。

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摘要

Effect of AKBA on cell proliferation and apoptosis in docetaxel-resistant PCa cells. The in vitro effect of docetaxel on established human docetaxel-resistant PC3/Doc cells and parental PC3 cells. ***  b Cell viability in response to AKBA was determined by the MTT assay after 48 h of treatment in PC3 and PC3/Doc cells. The results are the means ± SD of three independent experiments. *  c The morphological changes after 48 h of treatment with 0, 10, 20, and 30 μM AKBA in PC3 and PC3/Doc cells. AKBA-induced cell death was detected by annexin V/PI staining and flow cytometric analysis. The expression of PARP in cells treated with AKBA at various concentrations was examined by western blotting. GAPDH served as the loading control. Cell viability in the absence or presence of the pan-caspase inhibitor Z-VAD-fmk. PC3/Doc cells were exposed to 10 μM Z-VAD-fmk for 2 h prior to 20 μM AKBA or vehicle treatment. The results are the means ± SD of three independent experiments. **
机译:AKBA对多西他赛耐药PCa细胞增殖和凋亡的影响。多西紫杉醇对已建立的耐人多西紫杉醇的PC3 / Doc细胞和亲代PC3细胞的体外作用。 *** b在PC3和PC3 / Doc细胞中处理48µh后,通过MTT分析确定了对AKBA的反应细胞活力。结果是三个独立实验的平均值±SD。 * c在PC3和PC3 / Doc细胞中用0、10、20和30μmAKBA处理48 h后的形态变化。通过膜联蛋白V / PI染色和流式细胞仪分析检测到AKBA诱导的细胞死亡。通过蛋白质印迹法检测了用各种浓度的AKBA处理的细胞中PARP的表达。 GAPDH用作加载控件。在不存在或存在泛半胱天冬酶抑制剂Z-VAD-fmk的情况下的细胞活力。在20μmAKBA或载体处理之前,将PC3 / Doc细胞暴露于10μmZ-VAD-fmk中2μh。结果是三个独立实验的平均值±SD。 **

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