姜黄素抗体阵列治疗H69AR肺癌细胞后凋亡蛋白谱

S. Ilhan
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引用次数: 1

摘要

目的:探讨姜黄素(curcumin, Cur)治疗多重耐药H69AR非小细胞肺癌细胞后凋亡相关蛋白表达水平的变化。材料与方法:采用MTT法测定5-100µg/mL的Cur对H69AR细胞24、48、72 h的活性,ELISA法测定细胞凋亡。利用人凋亡抗体阵列对乳腺癌细胞系细胞凋亡相关蛋白进行分析。利用STRING数据库分析和可视化蛋白质之间的相互作用。结果:Cur抑制H69AR细胞活力,诱导细胞凋亡。在H69AR细胞中,Cur的IC50值为8.75µg/ mL。阵列结果显示,H69AR细胞中Bad、Bax、Caspase-3、TRAIL R1、TRAIL R2、FADD、Fas、SMAC/DIABLO、HMOX2等促凋亡蛋白水平显著提高了2.4-、3.1-、2.6-、3.1-、3.4-、2.4-、2.1-、4.1-和5.5倍(p<0.05)。此外,在H69AR细胞中,抗凋亡蛋白Bcl-2、cIAP-1、CLU和HIF1A的蛋白水平分别显著降低4.1倍、3.2倍、2.2倍和2.0倍(p<0.05)。结论:本研究结果提示,Cur通过介导多种参与外源性和内源性凋亡通路的蛋白介导人H69AR细胞凋亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Profile of Apoptotic Proteins after Curcumin Treatment by Antibody Array in H69AR Lung Cancer Cells
Objective: The aim of the study was to investigate the changes in the expression levels of apoptosis-related proteins after treatment with curcumin (Cur) on multiple drug-resistant H69AR non-small cell lung cancer cells. Materials and Methods: Viability of H69AR cells after Cur exposure (5-100 µg/mL) was evaluated via MTT assay at 24, 48 and 72 h. Apoptosis was assessed via ELISA assay. Apoptosis related proteins of breast cancer cell lines were analyzed by a Human Apoptosis Antibody Array. Protein-protein interactions were analyzed and visualized by using the STRING database. Results: Cur inhibited cell viability and induced apoptosis in H69AR cells. The IC50 value of Cur in H69AR cells was 8.75 µg/ mL. The array results showed that the protein levels of pro-apoptotic proteins such as Bad, Bax, Caspase-3, TRAIL R1, TRAIL R2, FADD, Fas, SMAC/DIABLO, HMOX2 were significantly increased by 2.4-, 3.1-, 2.6-, 3.1-, 3.4-, 2.4-, 2.1-, 4.1- and 5.5-fold in H69AR cells (p<0.05). Moreover, the protein levels of the anti-apoptotic proteins such as Bcl-2, cIAP-1, CLU and HIF1A were significantly decreased by 4.1-, 3.2-, 2.2- and 2.0-fold, respectively in H69AR cells by Cur exposure (p<0.05). Conclusion: Findings of this study suggested that Cur induced apoptosis of human H69AR cells via mediating several proteins involved in both extrinsic and intrinsic apoptotic pathways.
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