Differential inhibitory effects of TGF-β on EGF-, PDGF-, and HBGF-1-stimulated MG63 human osteosarcoma cell growth: Possible involvement of growth factor interactions at the receptor and postreceptor levels
✍ Scribed by Hiroyuki Mioh; Jan-Kan Chen
- Publisher
- John Wiley and Sons
- Year
- 1989
- Tongue
- English
- Weight
- 980 KB
- Volume
- 139
- Category
- Article
- ISSN
- 0021-9541
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✦ Synopsis
The growth of MG63 human osteosarcoma cell line in 5 % serum is stimulated by epidermal growth factor (EGF), platelet-derived growth factor (PDGF), or heparinbinding growth factor-1 (HBGF-1). The mitogenic effect of EGF and PDGF is completely blocked by TFG-f3 at 1 ng per ml and the effect of HBGF-1 is attenuated by 75-80%. Treatment of MG63 cells with TGF-P reduces HBGF-1 receptor binding affinity from 1.24 x lo-" M to 3.51 x lo-'' M with no change on the receptor number (1 . l . x 1 O3 per cell). The receptor-binding affinity of EGF and PDGF is not altered by TGF-P 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-P pretreatment. No change in the cellular protein tyrosine phosphorylation pattern can be detected in HBGF-1 -stimulated cells with and without TGF-P pretreatment. These data suggest that TGF-P inhibits EGF and PDGF mitogenicity by blocking EGFand PDGF-stimulated tyrosine kinase activity and attenuates HBGF-1 mitogenicity by decreasing its receptor affinity.