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

World J Gastroenterol. 2010 Apr 21;16(15):1859-66. doi: 10.3748/wjg.v16.i15.1859.

Abstract

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.

Keywords: Esophageal cancer; Migration; Proliferation; Sphingosine 1-phosphate; Sphingosine 1-phosphate 5.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation*
  • Dose-Response Relationship, Drug
  • Epithelium / pathology
  • Esophagus / cytology
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Lysophospholipids / metabolism
  • Mice
  • Mucous Membrane / pathology
  • Protein Binding
  • Receptors, Lysosphingolipid / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Sphingosine / analogs & derivatives
  • Sphingosine / metabolism
  • Transfection

Substances

  • Lysophospholipids
  • Receptors, Lysosphingolipid
  • sphingosine 1-phosphate
  • Sphingosine