DIFFERENTIAL CONTROL OF EXPRESSION OF TYPE-I AND TYPE-II RECEPTORS OFTRANSFORMING GROWTH-FACTOR-BETA IN COLON-CARCINOMA CELLS

We investigated TGF-beta response and the expression of TGF-beta recep tors in clones of MOSER colon carcinoma cells (designated MOSER II and MOSER III-10) as a function of their growth state. TGF-beta(1) respon se as assessed by induction of fibronectin expression was higher (3.0- fold) in exponentially growing cells than in quiescent cells. The expr ession of type I receptor (RI) mRNA was greater (2.5 to 3.0-fold) in e xponentially growing cells than in quiescent cells. In contrast, the e xpression of type II receptor (RII) mRNA was marginally increased in q uiescent cells relative to exponential cells. Nuclear run-off assays, and actinomycin-D treatment indicated that the increased expression of RI mRNA in exponentially growing cells was primarily due to an increa se in transcription, while a marginal increase in mRNA level for RII i n quiescent cells was primarily due to an increase in mRNA stability. Affinity cross-linking with I-125-labeled TGF-beta(1) showed that the exponentially growing cells displayed greater amounts of I-125 TGF-bet a(1) binding to RI and RII than quiescent cells, indicating that incre ased cell surface expression of receptors was correlated with increase d response in the exponential growth state. Immunoblot analysis also i ndicated greater amounts of RI protein in exponential compared to quie scent cells; however, no difference in RII protein was observed in the two growth states. These data indicate that expression of the recepto rs responsible for TGF-beta signal transduction are differentially con trolled. (C) 1996 Wiley-Liss, Inc.