KLF5 promotes cell migration by up-regulating FYN in bladder cancer cells

被引：33
|
作者：
Du, Chong [1 ]
Gao, Yang [1 ]
Xu, Shan [1 ,2 ]
Jia, Jing [1 ]
Huang, Zhixin [1 ]
Fan, Jinhai [1 ,2 ]
Wang, Xinyang [1 ,2 ]
He, Dalin [1 ,2 ]
Guo, Peng [1 ,2 ]
机构：
[1] Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Urol, 277 West Yan Ta Rd, Xian 710061, Shaanxi, Peoples R China
[2] Minist Educ, Oncol Res Lab, Key Lab Environm & Genes Related Dis, Xian, Shaanxi, Peoples R China
来源：
FEBS LETTERS | 2016年 / 590卷 / 03期
基金：
中国国家自然科学基金;
关键词：
bladder cancer; cell migration; FAK; FYN; KLF5; FOCAL ADHESION KINASE; KRUPPEL-LIKE FACTOR-5; PROTEASOME DEGRADATION; IMPORTANT MOLECULE; PROLIFERATION; TUMORIGENESIS; EXPRESSION; INDUCTION; INVASION; TARGET;
D O I：
10.1002/1873-3468.12069
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Kruppel-like factor 5 (KLF5) promotes cell proliferation of bladder cancer. However, whether KLF5 regulates other cell processes in bladder cancer is not clear. We found that KLF5 increases cell migration and lamellipodia formation, expression of FYN and phosphorylation of FAK in bladder cancer cells. In addition, KLF5 promotes transcription of FYN through binding to its promoter. FYN overexpression rescues cell migration and lamellipodia formation reduced by KLF5 knockdown. Furthermore, the KLF5/FYN/p-FAK axis is necessary for lysophosphatidic acid (LPA) to promote cell migration. Our findings indicate that both KLF5 and FYN are important in the regulation of cell migration in bladder cancer cells. We propose the KLF5/FYN/pFAK axis as a potential therapeutic target in bladder cancer.
引用
收藏
页码：408 / 418
页数：11
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