Effect of S1P5 on proliferation and migration of human esophageal cancer cells

被引:38
作者
Hu, Wei-Min [1 ]
Li, Li [2 ]
Ing, Bao-Qian [2 ]
Zhao, Yong-Sheng [3 ]
Wang, Chao-Li [2 ]
Feng, Li [2 ]
Xie, Yong-En [2 ]
机构
[1] N Sichuan Med Coll, Dept Microbiol & Immunol, Nanchong 637007, Sichuan Prov, Peoples R China
[2] N Sichuan Med Coll, Inst Immunol & Mol Biol, Nanchong 637007, Sichuan Prov, Peoples R China
[3] N Sichuan Med Coll, Affiliated Hosp, Dept Thorac Surg, Nanchong 637007, Sichuan Prov, Peoples R China
关键词
Sphingosine; 1-phosphate; Esophageal cancer; 5; Proliferation; Migration; SPHINGOSINE 1-PHOSPHATE RECEPTOR; SPHINGOSINE-1-PHOSPHATE RECEPTORS; DIFFERENTIAL REGULATION; TRIMODALITY THERAPY; EXPRESSION PROFILE; FAMILY; CARCINOMA; ADHESION; INVASIVENESS; ACTIVATION;
D O I
10.3748/wjg.v16.i15.1859
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
AIM: To investigate the sphingosine 1-phosphate (S1P) receptor expression profile in human esophageal cancer cells and the effects of S1P5 on proliferation and migration of human esophageal cancer cells. METHODS: S1P receptor expression profile in human esophageal squamous cell carcinoma cell line Eca109 was detected by semi-quantitative reverse transcription polymerase chain reaction. Eca109 cells were stably transfected with S1P5-EGFP or control-EGFP constructs. The relation between the responses of cell proliferation and migration to S1P and S1P5 expression was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and migration assay, respectively. RESULTS: Both normal human esophageal mucosal epithelium and Eca109 cells expressed S1P1, S1P2, S1P3 and S1P5, respectively. Esophageal mucosal epithelium expressed S1P5 at a higher level than Eca109 cell line. S1P5 over-expressing Eca109 cells displayed spindle cell morphology with elongated and extended filopodia-like projections. The proliferation response of S1P5-transfected Eca109 cells was lower than that of control vector-transfected cells with or without S1P stimulation (P < 0.05 or 0.01). S1P significantly inhibited the migration of S1P5-transfected Eca109 cells (P < 0.001). However, without S1P in transwell lower chamber, the number of migrated S1P5-transfected Eca109 cells was greater than that of control vector-transfected Eca109 cells (P < 0.001). CONCLUSION: S1P binding to S1P5 inhibits the proliferation and migration of S1P5-transfected Eca109 cells. Esophageal cancer cells may down-regulate the expression of S1P5 to escape the inhibitory effect. (C) 2010 Baishideng. All rights reserved.
引用
收藏
页码:1859 / 1866
页数:8
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