Up-regulation of SRPK1 in non-small cell lung cancer promotes the growth and migration of cancer cells

被引:27
|
作者
Liu, Hongcheng [1 ]
Hu, Xuefei [1 ]
Zhu, Yuming [1 ]
Jiang, Gening [1 ]
Chen, Sheng [2 ]
机构
[1] Tongji Univ, Sch Med, Shanghai Pulm Hosp, Dept Thorac Surg, 507 Zhengmin Rd, Shanghai 200433, Peoples R China
[2] Huaian First Peoples Hosp, Dept Thorac Surg, Huaian, Peoples R China
关键词
NSCLC; SRPK1; Beta-catenin/TCF signaling; Cell growth and migration; EXPRESSION; AKT; SR; ANGIOGENESIS; RESISTANCE; CARCINOMA; AXIS;
D O I
10.1007/s13277-015-4510-z
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Dys-regulation of serine-arginine protein kinase 1 (SRPK1) has been reported in non-small cell lung cancer (NSCLC). However, its functions in the progression of NSCLC remain poorly understood. In this study, the expression of SRPK1 in NSCLC tissues was determined using real-time PCR, and the roles of SRPK1 in the progression of NSCLC were investigated. It was found that both the mRNA level and the protein level of SRPK1 were up-regulated in NSCLC tissues. Forced expression of SRPK1 promoted the growth and migration of NSCLC cells, while knocking down the expression of SRPK1 inhibited the growth, migration, and tumorigenicity of NSCLC cells. Mechanism studies showed that SRPK1 activated the transcriptional activity of beta-catenin/T-cell factor (TCF) complex, and knocking down the expression of SRPK1 attenuated the expression of target genes of beta-catenin/T-cell factor (TCF) complex. In addition, silencing the expression of SRPK1 down-regulated the phosphorylation of GSK3beta. Taken together, SRPK1 might play an oncogenic role in NSCLC, and SRPK1 might be a therapeutic target for NSCLC.
引用
收藏
页码:7287 / 7293
页数:7
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