title: Growth requirements and oncogene expression in the human thyroid cell line SGHTL-34.
abstract: The SV40 T-antigen-transfected human thyroid cell line SGHTL-34 was used to investigate the effect of thyrotropin (TSH), insulin-like growth factor-1 (IGF-1) and epidermal growth factor (EGF) on c-fos and c-erbB/EGF receptor (EGF-R) mRNA expression and their role in human thyroid cell proliferation. EGF caused a transient 8- and 4-fold increase in c-fos mRNA level after 30 min in serum/hormone-deprived and in logarithmically growing cells, respectively. EGF was only mitogenic in the presence of serum, as measured by 3H-thymidine incorporation and cell counting. TSH had no detectable effect on c-fos mRNA expression and no mitogenic effect on the SGHTL-34 cells. IGF-1 showed no effect alone or in combination with EGF or TSH on either proliferation or c-fos mRNA expression. Our data suggest that increased c-fos mRNA levels are part of the mitogenic pathway, but are insufficient to engender a mitogenic response. SGHTL-34 cells produced high levels of transforming growth factor-alpha (TGF-alpha) and c-erbB/EGF-R mRNA, also seen in thyroid papillary carcinomas. The TGF-alpha protein was detected in conditioned medium from the SGHTL-34 cells, indicating that TGF-alpha may function as an autocrine growth factor. Our data show that the c-erbB/EGF-R mRNA level is regulated by growth factors and hormones in the SGHTL-34 cell line. The SGHTL-34 cells may therefore represent a useful model system for studying the role of TGF-alpha and EGF-R in thyroid carcinogenesis.
authors.affiliation: Department of Biochemistry and Molecular Biology, University of Bergen, Norway.
authors.forename: G O
authors.initials: GO
authors.lastname: Ness
authors.forename: R
authors.initials: R
authors.lastname: Aasland
authors.forename: J R
authors.initials: JR
authors.lastname: Lillehaug
mesh_terms: D000952:Antigens, Polyomavirus Transforming / Q000096:biosynthesis; D002455:Cell Division / Q000187:drug effects*; D002460:Cell Line; D003513:Cycloheximide / Q000494:pharmacology; D004247:DNA / Q000096:biosynthesis; D004815:Epidermal Growth Factor / Q000494:pharmacology*; D066246:ErbB Receptors / Q000096:biosynthesis*; D015870:Gene Expression / Q000187:drug effects*; D016762:Genes, fos / Q000187:drug effects*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology*; D007700:Kinetics; D011518:Proto-Oncogene Proteins / Q000096:biosynthesis*; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis; D011519:Proto-Oncogenes / Q000187:drug effects*; D012333:RNA, Messenger / Q000096:biosynthesis; D018719:Erb-b2 Receptor Tyrosine Kinases; D013539:Simian virus 40 / Q000235:genetics; D013936:Thymidine / Q000378:metabolism; D013961:Thyroid Gland; D013972:Thyrotropin / Q000494:pharmacology*; D013997:Time Factors; D014162:Transfection
chemical_list: D000952:Antigens, Polyomavirus Transforming; D003513:Cycloheximide; D004247:DNA; D004815:Epidermal Growth Factor; D066246:ErbB Receptors; D007334:Insulin-Like Growth Factor I; D011518:Proto-Oncogene Proteins; D016760:Proto-Oncogene Proteins c-fos; D012333:RNA, Messenger; D018719:Erb-b2 Receptor Tyrosine Kinases; D013936:Thymidine; D013972:Thyrotropin