Advanced

Expression of sphingosine kinase gene in the interactions between human gastric carcinoma cell and vascular endothelial cell

Ren, J; Dong, L; Xu, Cang-Bao LU and Pan, BR (2002) In World Journal of Gastroenterology 8(4). p.602-607
Abstract
AIM: 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... (More)
AIM: 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. CONCLUSION: 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. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
World Journal of Gastroenterology
volume
8
issue
4
pages
602 - 607
publisher
WJG Press
external identifiers
  • wos:000177562800006
  • pmid:12174364
  • scopus:0036674227
ISSN
1007-9327
language
English
LU publication?
yes
id
c9163aee-d5b3-4279-a103-97ff7ae2c01e (old id 330225)
alternative location
http://www.wjgnet.com/1007-9327/8/602.asp
date added to LUP
2007-11-12 10:38:24
date last changed
2017-01-01 04:56:49
@article{c9163aee-d5b3-4279-a103-97ff7ae2c01e,
  abstract     = {AIM: 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&lt;0.01). The CM of HGCC could stimulate the growth of HVEC (2.70 +/- 0.01, P&lt;0.01) while the CM of HVEC could inhibit the growth of HGCC (52.97 +/- 0.01%, P&lt;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. CONCLUSION: 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.},
  author       = {Ren, J and Dong, L and Xu, Cang-Bao and Pan, BR},
  issn         = {1007-9327},
  language     = {eng},
  number       = {4},
  pages        = {602--607},
  publisher    = {WJG Press},
  series       = {World Journal of Gastroenterology},
  title        = {Expression of sphingosine kinase gene in the interactions between human gastric carcinoma cell and vascular endothelial cell},
  volume       = {8},
  year         = {2002},
}