Effects of N,N‐dimethylformamide and extracellular matrix on transforming growth factor‐β binding to a human colon carcinoma cell line

Alterations in the binding of transforming growth factor‐β (TGF‐β) to the MOSER human colon carcinoma cell line caused by N, N‐dimethylformamide (DMF) or extracellular matrix (ECM) were examined. DMF induced a more differentiated phenotype in the MOSER cells and resulted in a twofold increase in TGF‐β binding to the cells. This was due to an increase in receptor number with no significant alteration in the KD. The extent of increased TGF‐β binding was dependent on the dose and time of exposure to DMF. Upon removal of DMF, the receptor level returned to that of untreated cells within 6 hr. The binding of TGF‐β1 and TGF‐β2 to the cells was increased equally. Despite this increase in TGF‐β binding in the presence of DMF, the sensitivity of the MOSER cells to the growth inhibitory effects of TGF‐β was unaltered. Growth of the MOSER cells on ECM derived from a well‐differentiated colon cell line increased the TGF‐β receptor number twofold without altering the KD. No change was observed if the MOSER cells were grown on ECM derived from a poorly differentiated cell line. While no alteration in sensitivity to TGF‐β was observed on cells grown in the presence of DMF, MOSER cells grown on the ECM derived from well‐differentiated colon carcinoma cell lines were twofold more sensitive to the growth inhibitory effects of TGF‐β. These results indicated that growth conditions which resulted in a more differentiated phenotype resulted in an increase in the cellular receptors for TGF‐β.