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姜黄素通过抑制自噬和凋亡来抑制非小细胞肺癌的发展。

Curcumin inhibits the development of non-small cell lung cancer by inhibiting autophagy and apoptosis.

作者信息

Wang Aili, Wang Jinxiang, Zhang Shuming, Zhang Hongxia, Xu Zhenyang, Li Xiaohui

机构信息

Department of Respiratory and Critical Care Medicine, Beijing Luhe Hospital, Capital Medical University, Beijing 101100, P.R. China.

出版信息

Exp Ther Med. 2017 Nov;14(5):5075-5080. doi: 10.3892/etm.2017.5172. Epub 2017 Sep 21.

Abstract

Among patients with primary lung cancer, 75-80% present with non-small cell lung cancer (NSCLC). However, there is a lack of studies into the potential preventive effects of curcumin against the activation of autophagy in NSCLC. Therefore, the present study primarily focused on the protective role of curcumin in NSCLC. It was demonstrated that curcumin decreased the viability of the human lung cancer cells lines, A549 and H1299, in a time-and dose-dependent manner (P<0.05). Treatment with curcumin also suppressed the colony formation capacities of A549 and H1299 cells. Following incubation with 10 µM curcumin for 48 h, cell apoptosis was significantly increased by 2.35- and 3.02-fold in A549 and H1299 cells, respectively, when compared with controls (P<0.01). Furthermore, curcumin treatment markedly increased the number and volume of autophagosomes in A549 and H1299 cells when compared with controls. Treatment with 10 µM curcumin for 48 h also significantly reduced the phosphorylation levels of mechanistic target of rapamycin (mTOR), ribosomal protein S6, phosphoinositide 3-kinase and AKT (protein kinase B) in A549 and H1299 cells (P<0.05). These data indicated that curcumin enhanced autophagy and apoptosis in NSCLC cells by acting as an mTOR complex1/2 inhibitor.

摘要

在原发性肺癌患者中,75%-80%为非小细胞肺癌(NSCLC)。然而,关于姜黄素对NSCLC中自噬激活的潜在预防作用的研究较少。因此,本研究主要关注姜黄素在NSCLC中的保护作用。结果表明,姜黄素以时间和剂量依赖性方式降低人肺癌细胞系A549和H1299的活力(P<0.05)。姜黄素处理还抑制了A549和H1299细胞的集落形成能力。与对照组相比,用10μM姜黄素孵育48小时后,A549和H1299细胞的细胞凋亡分别显著增加了2.35倍和3.02倍(P<0.01)。此外,与对照组相比,姜黄素处理显著增加了A549和H1299细胞中自噬体的数量和体积。用10μM姜黄素处理48小时也显著降低了A549和H1299细胞中雷帕霉素机制靶点(mTOR)、核糖体蛋白S6、磷酸肌醇3激酶和AKT(蛋白激酶B)的磷酸化水平(P<0.05)。这些数据表明,姜黄素通过作为mTOR复合物1/2抑制剂增强了NSCLC细胞中的自噬和凋亡。

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