Abstract

Platelet derived growth factor (PDGF) and wortmannin are two well-known factors that have beenused to study the response of various types of cancer cells. Both are related to the expression andactivity of phosphatidylinositol 3-kinase (PI3K), and its effect on these tumor cells. Thephosphatidylinositol-3-kinase (PI3K) and the PDGF signaling pathways are both crucial to manyaspects of cell growth and survival, in physiological as well as in pathological conditions. The researchstudy aims to evaluate the effects and cellular response of T98G glioblastoma cells. Here we haveshown that cells dosed with platelet-derived-growth-factor (PDGF) and /or wortmannin, an inhibitor ofPI3 kinase, proliferated at expected rates with respect to cells deprived of any additions. Cells withadded platelet-derived-growth-factor (PDGF) multiplied substantially faster than naturally growingcells-some thirty percent. As anticipated, cells given only wortmannin divided over forty percent slowerthan cells without any dosage. Additionally, cells transfected with a luciferase reporter vector carryingconsensus sequences of the nuclear factor NF-κB and AP-1 demonstrated that wortmannin treatmentpartially blocked the activation and expression of the NF-κB luciferase, while the activation andexpression of the AP-1 reporter vector was clearly increase in T98G glioblastoma cells. However, theeffect of wortmannin on the expression of NF-κB reporter vector was not observed by PDFGtreatment. Our data indicate that Wortmannin and PDGF play different role in the control andexpression of Phosphoinositide 3-kinase and in the regulation of different nuclear factor.