S1P/S1P1 signaling stimulates cell migration and invasion in Wilms tumor.

TitleS1P/S1P1 signaling stimulates cell migration and invasion in Wilms tumor.
Publication TypeJournal Article
Year of Publication2009
AuthorsLi M-H, Sanchez T, Yamase H, Hla T, Oo MLin, Pappalardo A, Lynch KR, Lin C-Y, Ferrer F
JournalCancer Lett
Volume276
Issue2
Pagination171-9
Date Published2009 Apr 18
ISSN1872-7980
KeywordsCell Line, Tumor, Cell Movement, GTP-Binding Protein alpha Subunits, Gi-Go, Humans, Kidney Neoplasms, Lysophospholipids, Neoplasm Invasiveness, Phosphatidylinositol 3-Kinases, rac1 GTP-Binding Protein, Receptors, Lysosphingolipid, RNA, Small Interfering, Signal Transduction, Sphingosine, Wilms Tumor
Abstract

Sphingosine-1-phosphate (S1P) is an important regulator of cellular functions via interaction with its receptors S1P(1-5). To date, nothing is known about the S1P receptor expression and the effects of S1P signaling in Wilms tumor. In this study, we found ubiquitous expression of S1P receptors in Wilms tumor specimens and cell lines. We demonstrated that S1P(1) acted as a promigratory modulator by employing S1P(1) antagonist VPC44116, S1P(1) siRNA and adenoviral transduction in Wilms tumor cells. Further, we clarified that S1P(1)-mediated migration occurred via Gi coupling and activation of PI3K and Rac1. In addition, S1P stimulated WiT49 cell invasion through S1P(1)/Gi signaling pathway. We consider that targeting S1P(1) may be a point of therapeutic intervention in Wilms tumor.

DOI10.1016/j.canlet.2008.11.025
Alternate JournalCancer Lett
PubMed ID19131156
PubMed Central IDPMC2943759
Grant ListK08 DK070468-03 / DK / NIDDK NIH HHS / United States
K08 DK 070468 A / DK / NIDDK NIH HHS / United States
K08 DK070468 / DK / NIDDK NIH HHS / United States
R01 CA168903 / CA / NCI NIH HHS / United States
R01 GM067958-06 / GM / NIGMS NIH HHS / United States
R01 GM067958 / GM / NIGMS NIH HHS / United States
Related Faculty: 
Teresa Sanchez, Ph.D.

Pathology & Laboratory Medicine 1300 York Avenue New York, NY 10065 Phone: (212) 746-6464
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