title: Expression of sphingosine kinase gene in the interactions between human gastric carcinoma cell and vascular endothelial cell.
abstract: OBJECTIVE
  To study the interactions between human gastric carcinoma cell (HGCC) and human vascular endothelial cell (HVEC), and if the expression of sphingosine kinase(SPK) gene was involved in these interactions.
  
  
  METHODS
  The specific inhibitor to SPK, dimethyl sphingosine (DMS), was added acting on HGCC and HVEC, then the cell proliferation was measured by MTT. The conditioned mediums (CMs) of HGCC and HVEC were prepared. The CM of one kind of cell was added to the other kind of cell, and the cell proliferation was measured by MTT. After the action of CM, the cellular expression of SPK gene in mRNA level was detected with in situ hybridization(ISH).
  
  
  RESULTS
  DMS could almost completely inhibit the proliferation of HGCC and HVEC. The growth inhibitory rates could amount to 97.21 %, 83.42 %, respectively (P<0.01). The CM of HGCC could stimulate the growth of HVEC (2.70+/-0.01, P<0.01) while the CM of HVEC could inhibit the growth of HGCC (52.97+/-0.01 %, P<0.01). There was no significant change in the mRNA level of SPK gene in one kind of cell after the action of the CM of the other kind of cell.
  
  
  CONCLUSIONS
  SPK plays a key role in regulating the proliferation of HGCC and HVEC. There exist complicated interactions between HGCC and HVEC. HGCC can significantly stimulate the growth of HVEC while HVEC can significantly inhibit the growth of HGCC. The expression of SPK gene is not involved in the interactions.
authors.affiliation: Department of Oncological Radiotherapy, First Hospital,Xi'an Jiaotong University Xi'an 710061, Shaanxi Province, China. renjuan88@163.net
authors.forename: Juan
authors.initials: J
authors.lastname: Ren
authors.forename: Lei
authors.initials: L
authors.lastname: Dong
authors.forename: Cang-Bao
authors.initials: CB
authors.lastname: Xu
authors.forename: Bo-Rong
authors.initials: BR
authors.lastname: Pan
mesh_terms: D002450:Cell Communication; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D017077:Culture Media, Conditioned; D004730:Endothelium, Vascular / Q000187:drug effects / Q000201:enzymology* / Q000473:pathology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D015870:Gene Expression; D006801:Humans; D017853:Phosphotransferases (Alcohol Group Acceptor) / Q000037:antagonists & inhibitors / Q000235:genetics*; D012333:RNA, Messenger / Q000235:genetics; D012334:RNA, Neoplasm / Q000235:genetics; D013110:Sphingosine / Q000031:analogs & derivatives* / Q000494:pharmacology; D013274:Stomach Neoplasms / Q000098:blood supply / Q000201:enzymology* / Q000235:genetics*; D014407:Tumor Cells, Cultured; D000099157:Sphingosine Kinase
chemical_list: D017077:Culture Media, Conditioned; D004791:Enzyme Inhibitors; D017853:Phosphotransferases (Alcohol Group Acceptor); D012333:RNA, Messenger; D012334:RNA, Neoplasm; D013110:Sphingosine; D000099157:Sphingosine Kinase; C061800:N,N-dimethylsphingosine