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首页> 外文期刊>Journal of cellular biochemistry. >Magnolol induces apoptosis via inhibiting the EGFR/PI3K/Akt signaling pathway in human prostate cancer cells.
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Magnolol induces apoptosis via inhibiting the EGFR/PI3K/Akt signaling pathway in human prostate cancer cells.

机译：厚朴酚通过抑制人前列腺癌细胞中的EGFR / PI3K / Akt信号传导途径诱导凋亡。

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摘要

We observed that treatment of prostate cancer cells for 24 h with magnolol, a phenolic component extracted from the root and stem bark of the oriental herb Magnolia officinalis, induced apoptotic cell death in a dose- and time-dependent manner. A sustained inhibition of the major survival signal, Akt, occurred in magnolol-treated cells. Treatment of PC-3 cells with an apoptosis-inducing concentration of magnolol (60 microM) resulted in a rapid decrease in the level of phosphorylated Akt leading to inhibition of its kinase activity. Magnolol treatment (60 microM) also caused a decrease in Ser((136)) phosphorylation of Bad (a proapoptotic protein), which is a downstream target of Akt. Protein interaction assay revealed that Bcl-xL, an anti-apoptotic protein, was associated with Bad during treatment with magnolol. We also observed that during treatment with magnolol, translocation of Bax to the mitochondrial membrane occurred and the translocation was accompanied by cytochrome c release, and cleavage of procaspase-8, -9, -3, and poly(ADP-ribose) polymerase (PARP). Similar results were observed in human colon cancer HCT116Bax(+/-) cell line, but not HCT116Bax(-/-) cell line. Interestingly, at similar concentrations (60 microM), magnolol treatment did not affect the viability of normal human prostate epithelial cell (PrEC) line. We also observed that apoptotic cell death by magnolol was associated with significant inhibition of pEGFR, pPI3K, and pAkt. These results suggest that one of the mechanisms of the apoptotic activity of magnolol involves its effect on epidermal growth factor receptor (EGFR)-mediated signaling transduction pathways.
机译：我们观察到用厚朴酚（一种从东方草药木兰的根和茎皮中提取的酚类成分）治疗前列腺癌细胞24小时，它以剂量和时间依赖性方式诱导凋亡性细胞死亡。在厚朴酚处理的细胞中持续抑制主要存活信号Akt。用细胞凋亡诱导浓度的厚朴酚（60 microM）处理PC-3细胞，导致磷酸化Akt的水平迅速下降，导致其激酶活性受到抑制。厚朴酚处理（60 microM）还导致Bad（一种促凋亡蛋白）的Ser（（136））磷酸化水平降低，而Bad（一种促凋亡蛋白）是Akt的下游靶标。蛋白质相互作用测定表明，抗凋亡蛋白Bcl-xL与厚朴酚治疗期间的Bad关联。我们还观察到在用厚朴酚治疗期间，发生了Bax易位到线粒体膜的情况，并且易位伴随着细胞色素c的释放以及procaspase-8，-9，-3和多聚（ADP-核糖）聚合酶（PARP）的裂解。 ）。在人类结肠癌HCT116Bax（+/-）细胞系中观察到相似的结果，但在HCT116Bax（-/-）细胞系中观察不到。有趣的是，在相似浓度（60 microM）下，厚朴酚治疗不会影响正常人前列腺上皮细胞（PrEC）系的生存能力。我们还观察到厚朴酚引起的凋亡细胞死亡与pEGFR，pPI3K和pAkt的显着抑制有关。这些结果表明厚朴酚的凋亡活性的机制之一涉及其对表皮生长因子受体（EGFR）介导的信号转导途径的影响。

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