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硼替佐米对人食管癌细胞的作用及机制研究

发表时间:2017-12-15  浏览量:1022  下载量:103
全部作者: 敖楠楠,陈倩萍,李明,王畅,刘赓
作者单位: 苏州大学医学部放射医学与防护学院
摘 要: 目的:研究蛋白酶体抑制剂硼替佐米对人食管癌细胞的作用,发现其可能影响的信号通路,并探寻其可能的作用机制。方法:选取食管癌TE-1和KYSE-150细胞为研究对象;利用噻唑蓝(MTT)比色法测定不同浓度、不同作用时间下硼替佐米对食管癌细胞增殖能力的影响;流式细胞仪检测不同浓度硼替佐米作用后食管癌细胞周期的变化;Annexin V-FITC/PI双染法检测不同浓度硼替佐米作用后食管癌细胞凋亡的变化;基因芯片和实时荧光定量PCR(quantitative real-time PCR,qRT-PCR)进一步发现硼替佐米可能的作用机制。结果:硼替佐米能使两种食管癌细胞的生存率降低,并且呈剂量、时间依赖性;硼替佐米处理24 h后可以使食管癌细胞发生G2/M期阻滞;硼替佐米处理24 h后可以使TE-1细胞凋亡率明显增加,48 h后可以使KYSE-150细胞凋亡率明显增加;基因芯片揭示硼替佐米可以影响包括蛋白酶体、内质网、Wnt和钙离子在内的多种信号通路。结论:硼替佐米能抑制食管癌细胞增殖,诱导G2/M期阻滞,促进凋亡,其机制可能与靶向包括UBD、CUL3、HDAC6和GADD45A等在内的多个基因有关。
关 键 词: 肿瘤学;食管癌;硼替佐米;G2/M期阻滞;细胞凋亡
Title: Effect and mechanism study of Bortezomib on human esophageal cancer cells
Author: AO Nannan, CHEN Qianping, LI Ming, WANG Chang, LIU Geng
Organization: School of Radiation Medicine and Protection, Medical College of Soochow University
Abstract: Objective: To study the effect of proteasome inhibitor Bortezomib on human esophageal cancer cell lines, investigate the possible signaling pathways targeted, and explore the potential mechanisms. Methods: Two human esophageal cancer cell lines, TE-1 and KYSE-150, were used in this study. The esophageal cancer cell viability was detected by MTT colorimetry method after Bortezomib treatment under different concentrations and times. The cell cycle distribution was examined by flow cytometry and the apoptosis was determined by Annexin V-FITC/PI double staining after Bortezomib treatment under different concentrations. The mRNA level of the genes targeted by Bortezomib was analyzed by microarray chips and quantitative real-time PCR (qRT-PCR). Results: The cell viability of two human esophageal cancer cell lines was inhibited by Bortezomib in a dose- and time-dependent manner. The treatment of Bortezomib led to G2/M arrest of esophageal cancer cell after 24 h. Bortezomib also obviously enhanced apoptosis in TE-1 after 24 h and in KYSE-150 after 48 h. Microarray chips revealed that multiple signaling pathways were targeted by Bortezomib, including proteasome, endoplasmic reticulum, Wnt and calcium ion. Conclusion: Bortezomib could suppress the cell viability, cause G2/M arrest and induce apoptosis in human esophageal cancer cells. The possible targets may involve multiple genes including UBD, CUL3, HDAC6 and GADD45A.
Key words: oncology; esophageal cancer; Bortezomib; G2/M arrest; apoptosis
发表期数: 2017年12月第23期
引用格式: 敖楠楠,陈倩萍,李明,等. 硼替佐米对人食管癌细胞的作用及机制研究[J]. 中国科技论文在线精品论文,2017,10(23):2584-2592.
 
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