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木香烃内酯诱导SK-MES 1人肺鳞癌细胞发生G1/S期阻滞并激活线粒体介导的凋亡途径。

Costunolide induces G1/S phase arrest and activates mitochondrial-mediated apoptotic pathways in SK-MES 1 human lung squamous carcinoma cells.

作者信息

Hua Peiyan, Zhang Guangxin, Zhang Yifan, Sun Mei, Cui Ranji, Li Xin, Li Bingjin, Zhang Xingyi

机构信息

Department of Thoracic Surgery, The Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China.

Department of Pathology, The Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China.

出版信息

Oncol Lett. 2016 Apr;11(4):2780-2786. doi: 10.3892/ol.2016.4295. Epub 2016 Mar 1.

DOI:10.3892/ol.2016.4295
PMID:27073552
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4812560/
Abstract

Despite the availability of several therapeutic options, a safer and more effective modality strategy is required for the treatment of lung cancer. Costunolide, a sesquiterpene lactone which isolated from the Saussurea lappa, has potent anticancer properties. In the present study, the effects of costunolide on cell viability, the cell cycle and apoptosis in SK-MES-1 human lung squamous carcinoma cells were investigated. Costunolide induced morphological changes and inhibited growth of SK-MES-1 cells growth. Flow cytometric analysis data demonstrated that costunolide significantly induced apoptosis of SK-MES-1 cells and induced cell cycle arrest at G1/S phase in a dose-dependent manner. Through upregulation in the expression of p53 and Bax, and downregulation in the expression of Bcl-2 and activation of caspase-3, costunolide-induced apoptosis was confirmed by western blot analysis. In addition, the significant loss of mitochondrial membrane potential indicated that costunolide may induce apoptosis via the mitochondria-dependent pathway in SK-MES-1 cells. These results highlight the potential effects of costunolide as an anti-cancer agent in a human lung squamous carcinoma cell line.

摘要

尽管有多种治疗选择,但治疗肺癌仍需要一种更安全、更有效的治疗策略。木香内酯是一种从木香中分离出来的倍半萜内酯,具有强大的抗癌特性。在本研究中,研究了木香内酯对SK-MES-1人肺鳞状癌细胞的细胞活力、细胞周期和凋亡的影响。木香内酯诱导形态变化并抑制SK-MES-1细胞的生长。流式细胞术分析数据表明,木香内酯以剂量依赖的方式显著诱导SK-MES-1细胞凋亡,并诱导细胞周期停滞在G1/S期。通过上调p53和Bax的表达,下调Bcl-2的表达并激活caspase-3,蛋白质免疫印迹分析证实了木香内酯诱导的凋亡。此外,线粒体膜电位的显著丧失表明木香内酯可能通过线粒体依赖性途径在SK-MES-1细胞中诱导凋亡。这些结果突出了木香内酯作为一种抗癌剂在人肺鳞状癌细胞系中的潜在作用。

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