Differential control of expression of type I and type II receptors of transforming growth factor-beta in colon carcinoma cells.

We investigated TGF-beta response and the expression of TGF-beta receptors in clones of MOSER colon carcinoma cells (designated MOSER II and MOSER III-10) as a function of their growth state. TGF-beta 1 response as assessed by induction of fibronectin expression was higher (3.0-fold) in exponentially growing cells than in quiescent cells. The expression of type I receptor (RI) mRNA was greater (2.5 to 3.0-fold) in exponentially growing cells than in quiescent cells. In contrast, the expression of type II receptor (RII) mRNA was marginally increased in quiescent 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 increase in transcription, while a marginal increase in mRNA level for RII in quiescent cells was primarily due to an increase in mRNA stability. Affinity cross-linking with 125I-labeled TGF-beta 1, showed that the exponentially growing cells displayed greater amounts of 125I TGF-beta 1 binding to RI and RII than quiescent cells, indicating that increased cell surface expression of receptors was correlated with increased response in the exponential growth state. Immunoblot analysis also indicated greater amounts of RI protein in exponential compared to quiescent cells; however, no difference in RII protein was observed in the two growth states. These data indicate that expression of the receptors responsible for TGF-beta signal transduction are differentially controlled.