Growth hormone induces insulin-like growth factor-I gene transcription by a synergistic action of STAT5 and HNF-1α

• Published in: FEBS letters Vol. 444; no. 2; pp. 155 - 159
• Main Authors: Metón, Isidoro, Boot, Elmieke P.J., Sussenbach, John S., Steenbergh, Paul H.
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 12.02.1999
• Subjects: GAS, γ-interferon-activated sequence; GH, growth hormone; GH-R, growth hormone receptor; HNF, hepatocyte nuclear factor; HNF-1; IGF, insulin-like growth factor; IGF-I; JAK, Janus kinase; Luc, luciferase; MEM, modified essential medium; Spi, serine protease inhibitor; STAT, signal transducer and activator of transcription; STAT5; TK, thymidine kinase; Transcription activation; GH; IGF-I; GAS, γ-interferon-activated sequence; STAT, signal transducer and activator of transcription; TK, thymidine kinase; HNF, hepatocyte nuclear factor; GH, growth hormone; MEM, modified essential medium; GH-R, growth hormone receptor; JAK, Janus kinase; Transcription activation; STAT5; IGF, insulin-like growth factor; Spi, serine protease inhibitor; HNF-1; Luc, luciferase
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/S0014-5793(99)00064-2

Salmon insulin-like growth factor-I (sIGF-I) expression is, as in mammals, induced by growth hormone (GH). To elucidate the mechanism by which GH stimulates the transcription of the IGF-I gene, we transiently transfected Hep3B cells expressing the rat GH receptor with a sIGF-I promoter-luciferase reporter construct. Activation of the construct by GH added to the medium of the transfected cells was observed when two specific transcription factors, STAT5 and HNF-1α, were simultaneously overexpressed in these cells. This finding demonstrates for the first time a GH-dependent activation of an IGF-I promoter construct in an immortalized laboratory cell line.