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γ-红没药烯通过诱导p53介导的线粒体凋亡对人神经母细胞瘤细胞的抗癌活性

Anticancer Activity of γ-Bisabolene in Human Neuroblastoma Cells via Induction of p53-Mediated Mitochondrial Apoptosis.

作者信息

Jou Yu-Jen, Hua Chun-Hung, Lin Chen-Sheng, Wang Ching-Ying, Wan Lei, Lin Ying-Ju, Huang Su-Hua, Lin Cheng-Wen

机构信息

Department of Medical Laboratory Science and Biotechnology, China Medical University, No. 91, Hsueh-Shih Road, Taichung 404, Taiwan.

Department of Otolaryngology, China Medical University Hospital, Taichung 404, Taiwan.

出版信息

Molecules. 2016 May 7;21(5):601. doi: 10.3390/molecules21050601.

DOI:10.3390/molecules21050601
PMID:27164076
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6272833/
Abstract

γ-Bisabolene has demonstrated antiproliferative activities against several human cancer cell lines. This study first discloses the antiproliferative and apoptosis induction activities of γ-bisabolene to human neuroblastoma TE671 cells. A CC50 value of γ-bisabolene was 8.2 μM to TE671 cells. Cell cycle analysis with PI staining showed γ-bisabolene elevating the sub-G1 fractions in a time-dependent manner. In addition, annexin V-FITC/PI staining showed γ-bisabolene significantly triggering early (annexin-V positive/PI negative) and late (annexin-V positive/PI positive) apoptosis in dose-dependent manners. γ-Bisabolene induced caspase 3/8/9 activation, intracellular ROS increase, and mitochondrial membrane potential decrease in apoptosis of human neuro-blastoma cells. Moreover, γ-bisabolene increased p53 phosphorylation and up-regulated p53-mediated apoptotic genes Bim and PUMA, as well as decreased the mRNA and protein levels of CK2α. Notably, the results indicated the involvement of CK2α-p53 pathways in mitochondria-mediated apoptosis of human neuroblastoma cells treated with γ-bisabolene. This study elucidated the apoptosis induction pathways of γ-bisabolene-treated neuroblastoma cells, in which could be useful for developing anti-neuroblastoma drugs.

摘要

γ-红没药烯已对多种人类癌细胞系表现出抗增殖活性。本研究首次揭示了γ-红没药烯对人神经母细胞瘤TE671细胞的抗增殖和诱导凋亡活性。γ-红没药烯对TE671细胞的CC50值为8.2 μM。用PI染色进行细胞周期分析表明，γ-红没药烯以时间依赖性方式提高亚G1期细胞比例。此外，膜联蛋白V-FITC/PI染色显示，γ-红没药烯以剂量依赖性方式显著触发早期（膜联蛋白-V阳性/PI阴性）和晚期（膜联蛋白-V阳性/PI阳性）凋亡。γ-红没药烯在人神经母细胞瘤细胞凋亡过程中诱导半胱天冬酶3/8/9激活、细胞内活性氧增加以及线粒体膜电位降低。此外，γ-红没药烯增加p53磷酸化并上调p53介导的凋亡基因Bim和PUMA，同时降低CK2α的mRNA和蛋白水平。值得注意的是，结果表明CK2α-p53通路参与了γ-红没药烯处理的人神经母细胞瘤细胞的线粒体介导的凋亡。本研究阐明了γ-红没药烯处理的神经母细胞瘤细胞的凋亡诱导途径，这可能有助于开发抗神经母细胞瘤药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5674/6272833/6df28f14edc9/molecules-21-00601-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5674/6272833/ae75d8a39d9c/molecules-21-00601-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5674/6272833/72bde9e76ed1/molecules-21-00601-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5674/6272833/b8b6ac5743c9/molecules-21-00601-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5674/6272833/6df28f14edc9/molecules-21-00601-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5674/6272833/ae75d8a39d9c/molecules-21-00601-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5674/6272833/8ad637b0a738/molecules-21-00601-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5674/6272833/2eba11d14e25/molecules-21-00601-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5674/6272833/a449e4f2e73f/molecules-21-00601-g004a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5674/6272833/72bde9e76ed1/molecules-21-00601-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5674/6272833/b8b6ac5743c9/molecules-21-00601-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5674/6272833/6df28f14edc9/molecules-21-00601-g007.jpg

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