Interaction of transforming growth factor-beta (TGF-beta) and epidermal growth factor (EGF) in human glioma cells.

摘要: Gliomas are characterized by a deregulation of growth factor production and receptors expression, e.g. overproduction the cytokine transforming factor-beta (TGF-beta) overexpression/constitutive activation for epidermal (EGF). Potential interactions such factors their signaling cascades could enhance malignancy these tumors. Therefore, we investigated effects TGF-beta EGF alone in combination on proliferation glioma cells cultivated from eight solid human WHO grade IV gliomas one cell line, analyzed expression intactness TGF-beta-signaling molecules Samd-4 -2, phosphorylation EGF-signaling kinases ERK 1/2. The were divergent complex: Whereas mostly stimulated proliferation, either enhanced, inhibited or had no significant effect proliferation. In combination, co-stimulation inhibition EGF-induced mitogenic activity be observed. Smad-4/-2 expressed all cells, point mutation at base 1595 Smad-4 did not affect its protein sequence. part reduced 1/2 cyclin-dependent kinase inhibitor 1 p21 was observed experiments. These experiments show that can inhibit EGF-mediated only some gliomas, whereas it enhances others. interaction both is very complex varies between different gliomas.