Shoichiro Ikuyama

Thyrotropin receptor gene expression in oncogene-transfected rat thyroid cells: Correlation between transformation, loss of thyrotropin-dependent growth, and loss of thyrotropin receptor gene expression

Rat FRTL-5 and PC-Cl-3 thyroid cells are continuously cultured, clonal lines which require thyrotropin to grow and function. Both can be efficiently transformed when infected with RNA or DNA viruses carrying oncogenes or when directly transfected with activated oncogenes. Transformation, assayed by the appearance of cell growth in agar and by tumorigenicity in syngeneic rats or nude mice, is associated with the loss of thyrotropin-dependent cell division and thyrotropin-regulated functions such as thyroglobulin synthesis. In 16 clones of FRTL-5 or PC-Cl-3 cells transformed with different oncogenes, we show that loss of thyrotropin-dependent growth and function correlates with the loss of thyrotropin receptor gene expression, measured with a rat thyrotropin receptor cDNA probe.

Structure and Regulated Expression of the TSH Receptor Gene: Differences and Similarities to Gonadotropin Receptors

Glycoprotein hormones—lutropin/chorionic gonadotropin (LH/CG), follicle stimulating hormone (FSH), and thyrotropin (TSH)—have a high degree of primary and tertiary structure similarity, yet are target tissue specific (1–5). The structural similarities of the hormones are complemented by functional similarities (1–5). Thus, all are well recognized to activate the cAMP signal transducing system, and all modulate both growth and differentiation of their respective target tissues. It is increasingly evident, in addition, that all depend on the action of other hormones, such as insulin and insulin-like growth factor I (IGF-I), to regulate growth and differentiated function (6–8).