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首页> 外文期刊>Archives of Toxicology >Dioscin-induced autophagy mitigates cell apoptosis through modulation of PI3K/Akt and ERK and JNK signaling pathways in human lung cancer cell lines
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Dioscin-induced autophagy mitigates cell apoptosis through modulation of PI3K/Akt and ERK and JNK signaling pathways in human lung cancer cell lines

机译：薯os素诱导的自噬通过调节人肺癌细胞系中的PI3K / Akt和ERK和JNK信号通路来减轻细胞凋亡

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Our previous study has revealed that dioscin, a compound with anti-inflammatory, lipid-lowering, anticancer and hepatoprotective effects, may induce autophagy in hepatoma cells. Autophagy is a lysosomal degradation pathway that is essential for cell survival and tissue homeostasis. In this study, the role of autophagy and related signaling pathways during dioscin-induced apoptosis in human lung cancer cells was investigated. Results from 4′-6-diamidino-2-phenylindole and annexin-V/PI double-staining assay showed that caspase-3- and caspase-8-dependent, and dose-dependent apoptoses were detected after a 24-h dioscin treatment. Meanwhile, autophagy was detected as early as 12 h after an exposure to low-dose dioscin, as indicated by an up-regulated expression of LC3-II and beclin-1 proteins. Blockade of autophagy with bafilomycin A1 or 3-methyladenine sensitized the A549 and H1299 cells to apoptosis. Treatment of A549 and H1299 cells with dioscin caused a dose-dependent increase in ERK1/2 and JNK1/2 activity, accompanied with a decreased PI3K expression and decreased phosphorylation of Akt and mTOR. Taken together, this study demonstrated for the first time that autophagy occurred earlier than apoptosis during dioscin-induced human lung cancer cell line apoptosis. Dioscin-induced autophagy via ERK1/2 and JNK1/2 pathways may provide a protective mechanism for cell survival against dioscin-induced apoptosis to act as a cytoprotective reaction.
机译：我们以前的研究表明，薯os皂素是一种具有抗炎，降脂，抗癌和保肝作用的化合物，可诱导肝癌细胞自噬。自噬是一种溶酶体降解途径，对细胞存活和组织稳态至关重要。在这项研究中，自噬和相关信号通路在薯os素诱导人肺癌细胞凋亡过程中的作用进行了研究。 4'-6-二mid基-2-苯基吲哚和膜联蛋白-V / PI双染色试验的结果表明，在24小时的薯os处理后，检测到caspase-3和caspase-8依赖性和剂量依赖性凋亡。同时，正如LC3-II和beclin-1蛋白表达上调所表明的，自暴露于低剂量薯di皂素后的12小时就检测到自噬。用bafilomycin A1或3-甲基腺嘌呤阻断自噬使A549和H1299细胞对细胞凋亡敏感。用薯os皂素处理A549和H1299细胞会导致ERK1 / 2和JNK1 / 2活性呈剂量依赖性增加，同时PI3K表达降低，Akt和mTOR磷酸化降低。两者合计，这项研究首次证明自吞噬发生在薯os素诱导的人肺癌细胞系凋亡过程中比凋亡更早。通过ERK1 / 2和JNK1 / 2途径诱导的薯os素自噬可能为细胞存活提供保护机制，以抵抗薯os素诱导的细胞凋亡，从而起到细胞保护作用。

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