KLF5 promotes cell migration by up-regulating FYN in bladder cancer cells
KLF5 promotes cell migration by up-regulating FYN in bladder cancer cells
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DOI：
10.1002/1873-3468.12069
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发表时间：
2016-02-01
期刊：
影响因子：
3.5
通讯作者：
Guo, Peng
中科院分区：
文献类型：
--
作者：
Du, Chong;Gao, Yang;Guo, Peng
Kruppel-like factor5(KLF5)促进膀胱癌细胞增殖。然而，KLF5是否调控膀胱癌的其他细胞过程尚不清楚。我们发现KLF5促进了膀胱癌细胞的迁移和片状脂体的形成，促进了FYN的表达和FAK的磷酸化。此外，KLF5通过与其启动子结合来促进FYN的转录。Fyn过表达挽救了KLF5基因敲除所减少的细胞迁移和板脂形成。此外，KLF5/FYN/p-FAK轴是溶血磷脂酸(LPA)促进细胞迁移所必需的。我们的研究结果表明，KLF5和FYN在膀胱癌细胞的迁移调控中都起着重要作用。我们建议KLF5/FYN/pFAK轴作为膀胱癌的潜在治疗靶点。
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.