Inhibition of cell proliferation by wortmannin in T98G cells involved induced inhibition of NF-kB transcriptional activity

Abstract

Wortmannin is an important regulator of Phosphoinositide 3-kinase (PI(3)K) signaling pathway. Changes in expression and activity of PI3-kinase and PDGF are major positive and negative regulators, respectively, of the PI3-kinase pathway, which regulates growth, survival, and proliferation. Here we have shown that cells dosed with platelet-derived-growth-factor (PDGF) and /or wortmannin, an inhibitor of PI3 kinase, proliferated at expected rates with respect to cells deprived of any additions. Cells with added platelet-derived-growth-factor (PDGF) multiplied substantially faster than naturally growing cells-some thirty percent. As anticipated, cells given only wortmannin divided over forty percent slower than cells without any dosage. Additionally, cells transfected with a luciferase reporter carrying a consensus sequences of the nuclear factor NF-κB binding site and treated with wortmannin inhibited the activation of luciferase in T98G cells. However, this inhibition was not affected by the treatment of PDFG. Our data indicate that Wortmannin and PDGF play different role in the control of expression of Phosphoinositide 3-kinase in glioma T98G cell line. *Correspondence to: Eduardo Parra, Laboratorio de Biomedicina Experimental, Escuela de Medicina, Universidad de Tarapacá. Campus Saucache, Edificio de la Escuela de Medicina, Avenida Senador Luis Alberto Rossi, Arica, Chile, E-mail: eparraarica@gmail.com