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首页> 外文期刊>Cell death & disease. >Bruceine D induces lung cancer cell apoptosis and autophagy via the ROS/MAPK signaling pathway in vitro and in vivo
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Bruceine D induces lung cancer cell apoptosis and autophagy via the ROS/MAPK signaling pathway in vitro and in vivo

机译:Bruceine D通过在体外和体内通过ROS / MAPK信号通路诱导肺癌细胞凋亡和自噬

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Worldwide, lung cancer remains a leading cause of cancer mortality. Bruceine D (BD) has been shown to induce pancreatic cancer cell death via several different mechanisms. In this study, we demonstrated that BD inhibited lung cancer cell proliferation. Apoptosis and autophagy were the most important mechanisms involved in BD-induced lung cancer cell death, and complete autophagic flux was observed in A549 and NCI-H292 cells. In addition, BD significantly improved intracellular reactive oxygen species (ROS) levels. BD-mediated cell apoptosis and autophagy were almost inhibited in cells pretreated with N-acetylcysteine (NAC), an ROS scavenger. Furthermore, MAPK signaling pathway activation contributed to BD-induced cell proliferation inhibition and NAC could eliminate p-ERK and p-JNK upregulation. Finally, an in vivo study indicated that BD inhibited the growth of lung cancer xenografts. Overall, BD is a promising candidate for the treatment of lung cancer owing to its multiple mechanisms and low toxicity.
机译:全世界,肺癌仍然是癌症死亡率的主要原因。已显示Bruceine D(BD)通过几种不同的机制诱导胰腺癌细胞死亡。在这项研究中,我们证明了BD抑制肺癌细胞增殖。细胞凋亡和自噬是参与BD诱导的肺癌细胞死亡的最重要的机制,在A549和NCI-H292细胞中观察到完全的自噬通量。此外,BD显着改善细胞内反应性氧物质(ROS)水平。在用N-乙酰半胱氨酸(NAC),ROS清除剂预处理的细胞中几乎抑制了BD介导的细胞凋亡和自噬。此外,MAPK信号传导途径激活有助于BD诱导的细胞增殖抑制和NAC可以消除P-ERK和P-JNK上调。最后,体内研究表明,BD抑制肺癌异种移植物的生长。总体而言,由于其多种机制和低毒性,BD是一种有希望的肺癌治疗肺癌的候选者。

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