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海葵(Heteractis magnifica)中的毒液通过激活线粒体介导的途径诱导非小细胞肺癌 A549 细胞凋亡。

Venom present in sea anemone (Heteractis magnifica) induces apoptosis in non-small-cell lung cancer A549 cells through activation of mitochondria-mediated pathway.

机构信息

Department of Medical Biotechnology, School of Medicine, Flinders University of South Australia, Bedford Park, SA, 5042, Australia,

出版信息

Biotechnol Lett. 2014 Mar;36(3):489-95. doi: 10.1007/s10529-013-1402-4. Epub 2013 Nov 5.

Abstract

Lung cancer is a major cause of cancer deaths throughout the world and the complexity of apoptosis resistance in lung cancer is apparent. Venom from Heteractis magnifica caused dose-dependent decreases in survival of the human non-small-cell lung cancer cell line, as determined by the MTT and Crystal Violet assays. The H. magnifica venom induced cell cycle arrest and induced apoptosis of A549 cells, as confirmed by annexin V/propidium iodide staining. The venom-induced apoptosis in A549 cells was characterized by cleavage of caspase-3 and a reduction in the mitochondrial membrane potential. Interestingly, crude extracts from H. magnifica had less effect on the survival of non-cancer cell lines. In the non-cancer cells, the mechanism via which cell death occurred was through necrosis not apoptosis. These findings are important for future work using H. magnifica venom for pharmaceutical development to treat human lung cancer.

摘要

肺癌是全球癌症死亡的主要原因,肺癌细胞凋亡抵抗的复杂性是显而易见的。研究表明,来自美丽鹿角珊瑚的毒液可导致人非小细胞肺癌细胞系的生存能力呈剂量依赖性下降,这可通过 MTT 和结晶紫检测来确定。美丽鹿角珊瑚毒液可诱导 A549 细胞周期停滞并诱导其凋亡,这可通过 Annexin V/碘化丙啶染色来确认。毒液诱导 A549 细胞凋亡的特征是 caspase-3 的裂解和线粒体膜电位的降低。有趣的是,美丽鹿角珊瑚的粗提取物对非癌细胞系的生存能力影响较小。在非癌细胞中,细胞死亡的机制是通过坏死而不是凋亡。这些发现对于未来使用美丽鹿角珊瑚毒液进行药物开发以治疗人类肺癌的工作非常重要。

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