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首页> 外文期刊>World Journal of Oncology >Curcumin Induces Apoptosis in EJ Bladder Cancer Cells via Modulating C-Myc and PI3K/Akt Signaling Pathway
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Curcumin Induces Apoptosis in EJ Bladder Cancer Cells via Modulating C-Myc and PI3K/Akt Signaling Pathway

机译：姜黄素通过调节C-Myc和PI3K / Akt信号通路诱导EJ膀胱癌细胞凋亡

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Background: Cancer chemopreventive agent curcumin has been shown to possess cell growth inhibition and apoptosis induction properties in several types of cancer. However, the detailed molecular mechanisms of the compound remain far from clear in EJ bladder cancer cells. Methods: The effect of curcumin on EJ cell growth and apoptosis was detected by MTT assays and flow cytometry. The phosphorylation levels of PTEN, PDK1, Akt, GSK-3β, c-Raf, and Bad and the expression levels of c-myc, Bax, Bcl-2, caspase-9, caspase-7, caspase-3, and PARP following curcumin administration were examined by immunoblots. Results: Curcumin suppressed the growth of EJ cells in a time and concentration dependent manner. Immunoblot showed that curcumin increased expression levels of c-myc and inhibited the activation of PI3K/Akt pathway in a time-dependent manner in EJ cells. Activation of PTEN, GSK-3β, c-Raf, caspase-9, caspase-7, and caspase-3, cleavage of PARP, upregulation of Bad and Bax, and downregulation of Akt and Bcl-2 were also found in curcumin-treated EJ cells. Conclusions: These findings establish a mechanistic linkup or interaction between c-myc, Bax, Bad, Bcl-2, caspase cascades, PI3K/Akt pathway and curcumin- induced apoptosis of EJ cells, suggesting that c-myc and PI3K/Akt signaling pathway play important roles in curcumin-induced apoptosis of EJ bladder cancer cells.doi:10.4021/wjon335w
机译：背景：癌症化学预防剂姜黄素已显示出在几种类型的癌症中具有细胞生长抑制和凋亡诱导特性。但是，该化合物的详细分子机制在EJ膀胱癌细胞中仍然不清楚。方法：采用MTT法和流式细胞术检测姜黄素对EJ细胞生长和凋亡的影响。 PTEN，PDK1，Akt，GSK-3β，c-Raf和Bad的磷酸化水平以及c-myc，Bax，Bcl-2，caspase-9，caspase-7，caspase-3和PARP的表达水平姜黄素的给药通过免疫印迹检查。结果：姜黄素以时间和浓度依赖性方式抑制EJ细胞的生长。免疫印迹显示姜黄素在EJ细胞中以时间依赖性方式增加c-myc的表达水平并抑制PI3K / Akt途径的激活。在姜黄素处理后，还发现PTEN，GSK-3β，c-Raf，caspase-9，caspase-7和caspase-3的激活，PARP的裂解，Bad和Bax的上调以及Akt和Bcl-2的下调。 EJ细胞。结论：这些发现建立了c-myc，Bax，Bad，Bcl-2，caspase级联，PI3K / Akt途径和姜黄素诱导的EJ细胞凋亡之间的机制联系或相互作用，表明c-myc和PI3K / Akt信号传导途径在姜黄素诱导的EJ膀胱癌细胞凋亡中起重要作用.doi：10.4021 / wjon335w

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