We have found that a G-protein coupled receptor FPR is selectively expressed by highly malignant human glioblastoma cells. Activation of FPR promotes tumor cell chemotaxis, survival and production of angiogenic facotr VEGF. Knocking down FPR by small interfering RNA markedly reduces the capacity of glioblastoma cells to form tumors in nude mice. In addition, FPR is activated by agonist activity contained in the supernatants of necrotic tumor cells. Thus, FPR acts as a sensor on glioblastoma cells for agonists produced in the tumor environment to exacerbate the progression of the tumor.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Intramural Research (Z01)
Project #
1Z01BC010724-02
Application #
7592882
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
2
Fiscal Year
2007
Total Cost
$270,473
Indirect Cost
Name
National Cancer Institute Division of Basic Sciences
Department
Type
DUNS #
City
State
Country
United States
Zip Code