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目的观察新型组蛋白去乙酰化酶抑制剂LBH589联合多烯紫杉醇(DCT)对人上皮性卵巢癌细胞细胞IGROV-1 Akt、mTOR、p70S6K蛋白表达的影响,探讨LBH589联合DCT诱导IGROV-1细胞凋亡的分子机制。方法采用不同浓度LBH589、DTX或两者联合处理IGROV-1细胞,用四甲基偶氮唑蓝(MTT)法检测细胞增殖活力,Western blot方法检测卵巢癌细胞IGROV-1 Akt、mTOR、p70S6K蛋白表达水平。结果 LBH589、DTX均能抑制IGROV-1细胞增殖,诱导凋亡,小剂量LBH589联合DTX作用更强。经Calcusyn软件分析证明两者联合具有明显的协同作用。Western blot结果显示LBH589联合DCT处理的IGROV-1细胞的Akt、mTOR、p70S6K蛋白水平均明显低于对照组。结论 Akt、mTOR、p70S6K通路可能在LBH589联合DCT诱导IGROV-1细胞凋亡中起作用。
Objective To investigate the effect of novel histone deacetylase inhibitor LBH589 combined with docetaxel (DCT) on the expression of IGROV-1 Akt, mTOR and p70S6K in human epithelial ovarian cancer cells and to investigate the effect of LBH589 and DCT on the apoptosis of IGROV-1 cells The molecular mechanism of death. Methods IGROV-1 cells were treated with different concentrations of LBH589, DTX or a combination of both. The proliferation of IGROV-1 cells was detected by MTT assay. The expressions of IGROV-1 Akt, mTOR and p70S6K proteins in ovarian cancer cells were detected by Western blot The expression level. Results Both LBH589 and DTX could inhibit the proliferation and induce apoptosis of IGROV-1 cells, and the effect of LBH589 and DTX was stronger. Calcusyn software analysis showed that the combination of the two has obvious synergies. Western blot results showed that the protein levels of Akt, mTOR and p70S6K in IGROV-1 cells treated with LBH589 and DCT were significantly lower than those in control group. Conclusion Akt, mTOR, p70S6K pathway may play a role in the apoptosis of IGROV-1 cells induced by LBH589 and DCT.