TGF-beta1 selectively suppresses PDGF receptor signaling pathways in MG-63 human osteosarcoma cell.
We previously found that TGF-beta1 inhibits PDGF mitogenicity in MG-63 cells and the inhibition is correlated with a suppression of the PDGF-induced receptor autophosphorylation. In this study, we analyze if all the PDGF receptor signaling pathways are similarly affected by the TGF-beta1 pretreatment. We show that TGF-beta1 suppresses PDGF-stimulated tyrosine phosphorylation of PLC-gamma1, and the phosphorylation of Erk. In contrast, the tyrosine phosphorylation of PI3-kinase is not affected. Thus, TGF-beta1 selectively suppresses two out of three PDGF receptor signaling pathways despite of its prominent inhibition of the PDGF-induced receptor autophosphorylation. The results also indicate that activation of the PI3-kinase pathway alone by PDGF is not sufficient in supporting the optimum growth of MG-63 cells under the culture conditions employed.
Hung
L M
LM
Department of Physiology, Chang Gung Medical College, Taoyuan, Taiwan.
Tsai
C H
CH
Chen
J K
JK
D006801:Humans; D012516:Osteosarcoma / Q000378:metabolism* / Q000473:pathology; D010766:Phosphorylation; D017479:Receptors, Platelet-Derived Growth Factor / Q000037:antagonists & inhibitors* / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D016212:Transforming Growth Factor beta / Q000494:pharmacology*; D014407:Tumor Cells, Cultured
D016212:Transforming Growth Factor beta; D017479:Receptors, Platelet-Derived Growth Factor