ISSN:
0021-9541
Keywords:
Life and Medical Sciences
;
Cell & Developmental Biology
Source:
Wiley InterScience Backfile Collection 1832-2000
Topics:
Biology
,
Medicine
Notes:
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.
Additional Material:
7 Ill.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1002/jcp.1041380304
