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Differential inhibitory effects of TGF-beta on EGF-, PDGF-, and HBGF-1-stimulated MG63 human osteosarcoma cell growth: possible involvement of growth factor interactions at the receptor and postreceptor levels.
J Cell Physiol. 1989 Jun; 139(3):509-16.JC

Abstract

The growth of MG63 human osteosarcoma cell line in 5% serum is stimulated by epidermal growth factor (EGF), platelet-derived growth factor (PDGF), or heparin-binding growth factor-1 (HBGF-1). The mitogenic effect of EGF and PDGF is completely blocked by TFG-beta at 1 ng per ml and the effect of HBGF-1 is attenuated by 75-80%. Treatment of MG63 cells with TGF-beta reduces HBGF-1 receptor binding affinity from 1.24 x 10(-11) M to 3.51 x 10(-11) M with no change on the receptor number (1.1 x 10(3) per cell). The receptor-binding affinity of EGF and PDGF is not altered by TGF-beta treatment; however, the number of EGF receptor is increased by 25%. Both EGF and PDGF stimulate MG63 cellular tyrosine kinase activity, and such stimulation is inhibited by TGF-beta pretreatment. No change in the cellular protein tyrosine phosphorylation pattern can be detected in HBGF-1-stimulated cells with and without TGF-beta pretreatment. These data suggest that TGF-beta inhibits EGF and PDGF mitogenicity by blocking EGF- and PDGF-stimulated tyrosine kinase activity and attenuates HBGF-1 mitogenicity by decreasing its receptor affinity.

Authors+Show Affiliations

Mioh H
W. Alton Jones Cell Science Center, Inc., Lake Placid, New York 12946.
Chen JK
No affiliation info available

MeSH

Cell DivisionCell LineCell MembraneEpidermal Growth FactorErbB ReceptorsFibroblast Growth Factor 1Growth SubstancesHeparinHumansKineticsMitogensMolecular WeightOsteosarcomaPhosphoproteinsPlatelet-Derived Growth FactorProtein-Tyrosine KinasesReceptors, Cell SurfaceReceptors, MitogenReceptors, Platelet-Derived Growth FactorReceptors, Vascular Endothelial Growth FactorTransforming Growth FactorsTumor Cells, Cultured

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

2472412

Citation

Mioh, H, and J K. Chen. "Differential Inhibitory Effects of TGF-beta On EGF-, PDGF-, and HBGF-1-stimulated MG63 Human Osteosarcoma Cell Growth: Possible Involvement of Growth Factor Interactions at the Receptor and Postreceptor Levels." Journal of Cellular Physiology, vol. 139, no. 3, 1989, pp. 509-16.
Mioh H, Chen JK. Differential inhibitory effects of TGF-beta on EGF-, PDGF-, and HBGF-1-stimulated MG63 human osteosarcoma cell growth: possible involvement of growth factor interactions at the receptor and postreceptor levels. J Cell Physiol. 1989;139(3):509-16.
Mioh, H., & Chen, J. K. (1989). Differential inhibitory effects of TGF-beta on EGF-, PDGF-, and HBGF-1-stimulated MG63 human osteosarcoma cell growth: possible involvement of growth factor interactions at the receptor and postreceptor levels. Journal of Cellular Physiology, 139(3), 509-16.
Mioh H, Chen JK. Differential Inhibitory Effects of TGF-beta On EGF-, PDGF-, and HBGF-1-stimulated MG63 Human Osteosarcoma Cell Growth: Possible Involvement of Growth Factor Interactions at the Receptor and Postreceptor Levels. J Cell Physiol. 1989;139(3):509-16. PubMed PMID: 2472412.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Differential inhibitory effects of TGF-beta on EGF-, PDGF-, and HBGF-1-stimulated MG63 human osteosarcoma cell growth: possible involvement of growth factor interactions at the receptor and postreceptor levels. AU - Mioh,H, AU - Chen,J K, PY - 1989/6/1/pubmed PY - 1989/6/1/medline PY - 1989/6/1/entrez SP - 509 EP - 16 JF - Journal of cellular physiology JO - J Cell Physiol VL - 139 IS - 3 N2 - The growth of MG63 human osteosarcoma cell line in 5% serum is stimulated by epidermal growth factor (EGF), platelet-derived growth factor (PDGF), or heparin-binding growth factor-1 (HBGF-1). The mitogenic effect of EGF and PDGF is completely blocked by TFG-beta at 1 ng per ml and the effect of HBGF-1 is attenuated by 75-80%. Treatment of MG63 cells with TGF-beta reduces HBGF-1 receptor binding affinity from 1.24 x 10(-11) M to 3.51 x 10(-11) M with no change on the receptor number (1.1 x 10(3) per cell). The receptor-binding affinity of EGF and PDGF is not altered by TGF-beta treatment; however, the number of EGF receptor is increased by 25%. Both EGF and PDGF stimulate MG63 cellular tyrosine kinase activity, and such stimulation is inhibited by TGF-beta pretreatment. No change in the cellular protein tyrosine phosphorylation pattern can be detected in HBGF-1-stimulated cells with and without TGF-beta pretreatment. These data suggest that TGF-beta inhibits EGF and PDGF mitogenicity by blocking EGF- and PDGF-stimulated tyrosine kinase activity and attenuates HBGF-1 mitogenicity by decreasing its receptor affinity. SN - 0021-9541 UR - https://www.unboundmedicine.com/medline/citation/2472412/Differential_inhibitory_effects_of_TGF_beta_on_EGF__PDGF__and_HBGF_1_stimulated_MG63_human_osteosarcoma_cell_growth:_possible_involvement_of_growth_factor_interactions_at_the_receptor_and_postreceptor_levels_ DB - PRIME DP - Unbound Medicine ER -