首页 | 本学科首页   官方微博 | 高级检索  
     

硼替佐米对胰腺癌细胞增殖、凋亡及PI3K/Akt通路的影响
引用本文:白晓黎1,范 华1,陈宏伟2. 硼替佐米对胰腺癌细胞增殖、凋亡及PI3K/Akt通路的影响[J]. 现代肿瘤医学, 2019, 0(24): 4323-4328. DOI: 10.3969/j.issn.1672-4992.2019.24.001
作者姓名:白晓黎1  范 华1  陈宏伟2
作者单位:1.河南科技大学第一附属医院药剂科,河南 洛阳 471000;2.郑州大学附属洛阳中心医院消化内科,河南 洛阳 471000
基金项目:National Natural Science Foundation of China(No.U1504808);国家自然科学基金资助项目(编号:U1504808)
摘    要:目的:探讨硼替佐米(BTZ)对胰腺癌细胞增殖、凋亡及PI3K/Akt通路的影响。方法:体外培养人胰腺癌细胞株PANC-1细胞,分别给予硼替佐米(0,2,10,50,250 nmol/L)作用24 h,采用MTT法检测PANC-1细胞活力,采用Annexin V/PI双染法检测细胞凋亡情况,采用流式细胞术检测细胞周期,采用Western blot检测细胞凋亡及PI3K/Akt通路相关蛋白表达情况。结果:与0 nmol/L硼替佐米相比,不同浓度硼替佐米处理后,PANC-1细胞生长抑制率均显著升高(P<0.05),G0/G1期细胞比例均显著升高(P<0.05),细胞凋亡率显著升高(P<0.05),细胞中cleaved-caspase-3、Bax蛋白表达增高(P<0.05),Bcl-2、PI3K、p-Akt蛋白表达降低(P<0.05),且呈剂量依赖性;裸鼠成瘤实验中,不同浓度硼替佐米作用后,肿瘤瘤体质量显著降低(P<0.05),且呈剂量依赖性。结论:硼替佐米能抑制胰腺癌细胞PANC-1增殖,诱导其凋亡,推测硼替佐米可能通过调节PI3K/Akt通路,激活凋亡蛋白基因表达,抑制抗凋亡蛋白基因的表达,诱导PANC-1细胞凋亡。

关 键 词:胰腺癌  硼替佐米  细胞增殖  细胞凋亡  PI3K/Akt通路

The effects of bortezomib on proliferation,apoptosis and PI3K/Akt pathway of pancreatic cancer cells
Bai Xiaoli1,Fan Hua1,Chen Hongwei2. The effects of bortezomib on proliferation,apoptosis and PI3K/Akt pathway of pancreatic cancer cells[J]. Journal of Modern Oncology, 2019, 0(24): 4323-4328. DOI: 10.3969/j.issn.1672-4992.2019.24.001
Authors:Bai Xiaoli1  Fan Hua1  Chen Hongwei2
Affiliation:1.Department of Pharmacy,the First Affiliated Hospital of Henan University of Science and Technology,Henan Luoyang 471000,China;2.Department of Gastroenterology,Zhengzhou University Affiliated Luoyang Central Hospital,Henan Luoyang 471000,China.
Abstract:Objective:To investigate the effects of bortezomib (BTZ) on proliferation,apoptosis,and PI3K/Akt pathway of pancreatic cancer cells.Methods:Human pancreatic cancer cell line PANC-1 cells were cultured in vitro.They were given bortezomib treatment (0,2,10,50,250 nmol/L) respectively for 24 h.MTT assay was used to detect the viability of PANC-1 cells.Annexin V/PI double staining was used to detect apoptosis.Cell cycle was detected by flow cytometry.Western blot was used to detect apoptosis and PI3K/Akt pathway related protein expression.Results:Compared with 0 nmol/L BTZ,after treatment with bortezomib at different concentrations,the growth inhibition rate of PANC-1 cells increased significantly (P<0.05),the proportion of G0/G1 phase cells increased significantly (P<0.05),the apoptosis rate increased significantly (P<0.05),the expressions of cleaved-caspase-3 and Bax protein in the cells increased (P<0.05),the protein expressions of Bcl-2,PI3K,and p-Akt decreased (P<0.05),in dose-dependent manners.In the tumor-forming experiment of nude mice,the tumor mass was significantly decreased (P<0.05) in dose-dependent manners.Conclusion:Bortezomib can inhibit the proliferation and induce apoptosis of pancreatic cancer cell PANC-1.It is speculated that bortezomib may activate apoptotic protein gene expression,inhibit anti-apoptotic protein gene expression,and induce PANC-1 cell apoptosis by regulating PI3K/Akt pathway.
Keywords:pancreatic cancer   bortezomib   cell proliferation   apoptosis   PI3K/Akt pathway
点击此处可从《现代肿瘤医学》浏览原始摘要信息
点击此处可从《现代肿瘤医学》下载免费的PDF全文
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号