Abstract
The growth of the mouse mammary Shionogi carcinoma 115 (SC 115)-derived cell line (SC-3) is markedly stimulated by androgen through induction of a heparin-binding growth factor termed androgen-induced growth factor (AIGF). This androgen-induced growth is partly blocked by thyroid hormone(s) such as triidothyronine (T 3). Transforming growth factor β1 (TGFβ1) also inhibits the growth of SC-3 cells. Thus, we have investigated the possibility that T 3 exerts its inhibitory effects on SC-3 cell growth through an alteration in AIGF or TGFβ1 mRNA expression. Unexpectedly, T 3 failed to modulate the expression of AIGF mRNA. T 3 was also unable to significantly affect TGFβ1 mRNA levels in androgen-stimulated SC-3 cells. More importantly, a neutralizing antibody against TGFβ1 could not block T 3-dependent inhibition of androgen-induced SC-3 cell growth. However, the inhibitory ability of T 3 was potentiated by TGFβ1. In addition, T 3 treatment resulted in a significant inhibition of AIGF-induced DNA synthesis. Thus, T 3 treatment renders SC-3 cells somehow refractory to AIGF. The signal pathway for T 3 to reduce AIGF responsiveness may be shared by TGFβ1.
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