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Growth Hormone-induced Alteration in ErbB-2 Phosphorylation Status in 3T3-F442A Fibroblasts
Journal article   Open access   Peer reviewed

Growth Hormone-induced Alteration in ErbB-2 Phosphorylation Status in 3T3-F442A Fibroblasts

Sung-Oh Kim, Jon C.D Houtman, Jing Jiang, J. Michael Ruppert, Paul J Bertics and Stuart J Frank
The Journal of biological chemistry, Vol.274(50), pp.36015-36024
12/1999
DOI: 10.1074/jbc.274.50.36015
PMID: 10585492
url
https://doi.org/10.1074/jbc.274.50.36015View
Published (Version of record) Open Access

Abstract

The growth hormone receptor (GHR), a cytokine receptor superfamily member, requires the JAK2 tyrosine kinase for signaling. We now examine functional interactions between growth hormone (GH) and epidermal growth factor (EGF) in 3T3-F442A fibroblasts. Although EGF enhanced ErbB-2 tyrosine phosphorylation, GH, while causing retardation of its migration on SDS-polyacrylamide gel electrophoresis, decreased ErbB-2's tyrosine phosphorylation. GH-induced retardation was reversed by treatment of anti-ErbB-2 precipitates with both alkaline phosphatase and protein phosphatase 2A, suggesting that GH induced serine/threonine phosphorylation of ErbB-2. Both GH-induced shift in ErbB-2 migration and GH-induced MAP kinase activation were unaffected by a protein kinase C inhibitor but were blocked by the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1 (MEK1) inhibitor, PD98059. Notably, leukemia inhibitory factor, but not interferon-γ, also promoted ErbB-2 shift and mitogen-activated protein kinase activation. Cotreatment with EGF and GH versus EGF alone resulted in a 35% decline in acute ErbB-2 tyrosine 1248 autophosphorylation, a marked decline (approximately 50%) in DNA synthesis, and substantially decreased cyclin D1 expression. We conclude that in 3T3-F442A cells, 1) the GH-induced decrease in ErbB-2 tyrosine phosphorylation correlates with MEK1/mitogen-activated protein kinase activity and 2) GH antagonizes EGF-induced DNA synthesis and cyclin D1 expression in a pattern consistent with its alteration in ErbB-2 phosphorylation status.

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