Abstract
Inhibition of cell proliferation by wortmannin in T98G cells involved induced inhibition of NF-kB transcriptional activity
Highlights
Wortmannin is a cell-permeable, fungal metabolite that acts as a potent, selective and irreversible inhibitor of phosphatidylinositol 3-kinase (PI3K) [1,2,3]
In contrast to the effect of wortmannin, T98G glioblastoma cells treated only with PDGF, proliferate at more expected rates with respect to cells deprived of any additions (Control) Using the averages on the last counting day, we see that the addition of wortmannin to cells treated with PDGF accounts for a proliferation decrease of about 15888 (82876-66987), a number which equals the difference in averages between control cells (58654) and cells dosed with wortmannin only (41678)
From this data it can be inferred that wortmannin inhibits cells boosted with PDGF by the same amount as it inhibits control cells
Summary
Wortmannin is a cell-permeable, fungal metabolite that acts as a potent, selective and irreversible inhibitor of phosphatidylinositol 3-kinase (PI3K) [1,2,3]. This kinase Phosphoinositide-3-kinase phosphorylates PtdIns [4,5] P2 (Phosphatidylinositol 4,5-bisphosphate) to generate phosphatidylinositol 3,4,5-trisphosphate (PIP3). The fungal metabolite wortmannin is a potent inhibitor of the lipid and protein kinase activities of class I PI3Ks [1]. The receptors of PDGF exists in two forms of strong structural homology: PDGFRα and PDGFRβ It is normally expressed by the cells of the supporting tissue; it plays a role in embryonic development and tissue scarring [19].
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