胰腺癌BxPC3细胞中Src激酶对Notch-1活化的调节

基础医学与临床 ›› 2008, Vol. 28 ›› Issue (9): 964-968.

胰腺癌BxPC3细胞中Src激酶对Notch-1活化的调节

杨小燕张玉祥王泽生

首都医科大学基础医学院首都医科大学生物化学与分子生物学系

收稿日期:2008-05-13 修回日期:1900-01-01 出版日期:2008-09-25 发布日期:2008-09-25
通讯作者: 王泽生

Tyrosine kinase Src mediates Notch-1 activation in BxPC3 pancreatic cancer cells

Xiao-yan YANG, Yu-xiang ZHANG, Zhe-sheng WANG

Capital Medical University Capital Medical University

Received:2008-05-13 Revised:1900-01-01 Online:2008-09-25 Published:2008-09-25
Contact: Zhe-sheng WANG

摘要/Abstract

摘要： 目的探讨在胰腺癌细胞BxPC3中, Src激酶对Notch-1活化的影响。方法用siRNA干扰的方法分别抑制Notch-1和c-Src的表达；加入Src激酶抑制剂PP2抑制Src激酶活性；MTT法检测细胞的生长；用Western blot检测Notch-1蛋白活性形式NICD水平的变化。结果抑制Notch-1表达及抑制Src激酶活性可明显抑制BxPC3细胞生长；抑制Src激酶活性及抑制c-Src蛋白表达可下调Notch-1 NICD水平。结论 Src激酶在胰腺癌细胞BxPC3中促进Notch-1的活化，促进BxPC3细胞的生长。

关键词: 胰腺癌, BxPC3, Notch-1, Src, PP2

Abstract: Objective To observe the effect of tyrosine kinase Src on activating Notch-1 protein in pancreatic cancer cell line - BxPC3. Methods Notch-1 expression and c-Src expression were inhibited by siRNA interference, and the activation of Src was inhibited by its inhibitor PP2. The growth rate of BxPC3 cells was measured by MTT. The changes of Notch-1 NICD level and Src protein level were measured by Western blot. Results The growth of BxPC3 cells decreased after inhibiting Notch-1 expression, as well as the cells were treated with PP2. The level of Notch-1 NICD decreased both after inhibiting c-Src expression and after Src activation was inhibited by PP2. Conclusion In BxPC3 cells, tyrosine kinase Src promotes the level of Notch-1 NICD, which directly influences the cell growth.

Key words: pancreas cancer, BxPC3, Notch-1, Src, PP2

杨小燕张玉祥王泽生. 胰腺癌BxPC3细胞中Src激酶对Notch-1活化的调节[J]. 基础医学与临床, 2008, 28(9): 964-968.

Xiao-yan YANG; Yu-xiang ZHANG; Zhe-sheng WANG. Tyrosine kinase Src mediates Notch-1 activation in BxPC3 pancreatic cancer cells[J]. Basic & Clinical Medicine, 2008, 28(9): 964-968.

[1]	温开凤武威杰李学军. 外泌体与胰腺癌的发生发展、诊断和治疗[J]. 基础医学与临床, 2019, 39(9): 1351-1355.
[2]	田明白仲添张辉胡进静周文策. 胰腺癌发生发展诱因及相关机制的研究进展[J]. 基础医学与临床, 2015, 35(8): 1122-1125.
[3]	孙宇孙宁杨绍时宋国栋. 肿瘤干细胞作为胰腺癌治疗潜在靶点的研究进展 [J]. 基础医学与临床, 2014, 34(7): 1006-1009.
[4]	陈明毕琳琳赵芳王智泉干学东王扬淦. 拟胚体贴壁时间对小鼠胚胎干细胞心肌分化的影响[J]. 基础医学与临床, 2013, 33(9): 1118-1122.
[5]	厉胜廖泉赵玉沛. 胰腺癌分子靶向治疗的研究进展[J]. 基础医学与临床, 2010, 30(5): 557-560.
[6]	姚军钱翠娟. 过表达NOTCH-1抑制TNFα诱导的胃癌BGC-823细胞增殖抑制及凋亡[J]. 基础医学与临床, 2009, 29(7): 726-730.
[7]	陈加祥徐斯凡王晶磊杨俊玲秦海燕邹挺. PP60C-SRC/ERK1/2信号通路调节大鼠精原干细胞活性[J]. 基础医学与临床, 2009, 29(7): 678-682.
[8]	张娟余和芬张玉祥王泽生. Rab5在胰腺癌细胞BxPC3中对 Notch1活性的调节[J]. 基础医学与临床, 2008, 28(7): 723-728.
[9]	倪晓光赵晓航王贵齐白晓枫刘芳周兰萍赵平. 泛素－蛋白酶体途径降解胰腺癌细胞系中凝溶胶蛋白[J]. 基础医学与临床, 2008, 28(6): 535-538.
[10]	花瞻张远春贾振庚张震生. Her-2/neu、DPC4和p16在胰腺癌中的表达及其意义[J]. 基础医学与临床, 2008, 28(1): 48-52.
[11]	杨红（协和）钱家鸣张惠广郭涛. 胰腺癌300例临床特点分析[J]. 基础医学与临床, 2007, 27(7): 815-818.
[12]	李晓冬张峰马毓梅. 基因枪转导K-ras反义基因对胰腺癌细胞K-ras p21蛋白表达的影响[J]. 基础医学与临床, 2007, 27(5): 495-498.