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首页> 外文期刊>RSC Advances >Paris saponin I inhibits proliferation and promotes apoptosis through down-regulating AKT activity in human non-small-cell lung cancer cells and inhibiting ERK expression in human small-cell lung cancer cells
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Paris saponin I inhibits proliferation and promotes apoptosis through down-regulating AKT activity in human non-small-cell lung cancer cells and inhibiting ERK expression in human small-cell lung cancer cells

机译：巴黎皂苷I抑制扩散，通过降低人非小细胞肺癌细胞中的AKT活性并抑制人类小细胞肺癌细胞的ERK表达，促进细胞凋亡

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摘要

Paris Saponin I (PSI), a steroidal saponin derivative extracted from a traditional Chinese herbal Paris polyphylla , has shown cytotoxic effects on several tumor cell lines. However, the mechanisms of its antitumor activity especially for lung cancers remain to be elucidated. In this present investigation, we continue to explore the efficacy and mechanisms underlying the cytotoxic effects of PSI in lung cancer cell lines. Three non-small cell lung cancer (NSCLC) cells (H1299, H520, H460) and one small cell lung cancer (SCLC) cell (H446) were treated with PSI for the first time. PSI significantly induced cell cycle arrest at the G2/M phase and mitochondrial-related apoptosis NSCLC cells but not SCLC cells. Additionally, PSI reduced phosphorylation of AKT in NSCLC and ERK in SCLC in general. Interestingly, we observed that PSI influenced different signaling pathways among the four kinds of lung cancer cells. After PSI treatment, p38 MAPK and ERK activation were observed in H1299, while p38 MAPK increased and JNK decreased in H520. On the contrary, we found JNK activation in H460 cells with PSI. However, PSI upregulated the AKT activity and inhibited the JNK expression in H446 cells. The results indicate that PSI exhibits the cytotoxicity in different pathways depending on the cancer types.
机译：巴黎皂苷I（PSI），一种从中草药Paris Polyphylla中提取的甾体皂苷衍生物，对几种肿瘤细胞系显示了细胞毒性作用。然而，尤其是对肺癌的抗肿瘤活性的机制仍然待阐明。在本目前的调查中，我们继续探讨PSI在肺癌细胞系中pSI细胞毒性作用的疗效和机制。第一次用PSI处理三种非小细胞肺癌（NSCLC）细胞（H1299，H520，H460）和一个小细胞肺癌（SCLC）细胞（H446）。 PSI在G2 / M相和线粒体相关的细胞凋亡NMSCLC细胞中显着诱导细胞周期停滞，但不是SCLC细胞。另外，PSI通常减少了NSCLC中AKT的磷酸化和SCLC中的ERK。有趣的是，我们观察到PSI影响了四种肺癌细胞中的不同信号途径。在PSI处理后，在H1299中观察到P38 MAPK和ERK激活，而P38 MAPK增加和JNK在H520中降低。相反，我们发现使用PSI的H460细胞中的JNK激活。然而，PSI上调了AKT活性并抑制H446细胞中的JNK表达。结果表明PSI根据癌症类型表现出不同途径中的细胞毒性。

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