TGF-beta1 actions on FRTL-5 cells provide a model for the physiological regulation of thyroid growth

Oncogene
C CarneiroF Domínguez

Abstract

Little is known about the TGF-beta1 mechanism that promotes thyroid cell growth arrest. We assessed TGF-beta1 effects on Fisher rat thyroid cell line (FRTL-5). This allowed us to study TGF-beta1 action on thyroid cells in various physiological situations such as actively proliferating cells, resting cells stimulated to proliferate by the action of various mitogens, and resting cells. TGF-beta1 arrested proliferating FRTL-5 cells, increasing c-myc mRNA levels and reducing p27-free cyclin D1 protein levels, without affecting either the cellular content of p27 or the cyclin D1-p27 complexes. Moreover, TGF-beta1 treatment reduced the activity of cyclin E-CDK2 complexes and, consequently, pRB was found to be hypophosphorylated. TGF-beta1 prevented resting cells to enter in the cell cycle when stimulated with growing medium (newborn calf serum plus a mixture of five hormones) but not when TSH (thyroid stimulating hormone) plus IGF-1 (Insulin-like growth factor I) were used as mitogens. Both stimuli increased the levels of cyclins D1, D3 and E but TGF-beta1 had a greater effect in decreasing these cyclin levels in growing-medium stimulated cells than in TSH + IGF-1. This suggests that for FRTL-5 cells, the content of these cyclins mus...Continue Reading

Citations

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