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PMID: 2895499 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Absence of TGF-beta receptors and growth inhibitory responses in retinoblastoma cells.

Science (New York, N.Y.) ·Vol. 240 ·No. 4849 ·1988-04-08 ·Pages 196-9

Kimchi A, Wang XF, Weinberg RA, Cheifetz S, Massagué J

Abstract

The responses of retinoblastoma tumor cells and normal retinal cells to various growth inhibitory factors were examined. Whereas fetal retinal cells were highly sensitive to the antimitogenic effects of transforming growth factor beta 1 (TGF-beta 1), retinoblastoma tumor cell lines were all resistant to this factor. Binding assays and affinity labeling of these cells with radioiodinated TGF-beta 1 revealed that the cells did not have TGF-beta receptors. The retinoblastoma cells lacked the three affinity-labeled proteins of 65, 95, and 300 kilodaltons typically seen in human cell lines and thus differed from normal retinal cells and from other types of neuroectodermal tumors that display the normal pattern of receptors. Loss of TGF-beta receptors, which is a rare event among tumor cells, may represent one mechanism through which these cells escape from negative control and form retinoblastomas.

MeSH Terms
Cell Division Cell Line Humans Peptides/physiology Receptors, Cell Surface/physiology Receptors, Transforming Growth Factor beta Retina/cytology Retinoblastoma/pathology,physiopathology Transforming Growth Factors
Chemicals
Peptides Receptors, Cell Surface Receptors, Transforming Growth Factor beta Transforming Growth Factors
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Kimchi A
Department of Virology, Weizmann Institute of Science, Rehovot, Israel.
Wang X F
Weinberg R A
Cheifetz S
Massagué J
Article Info
Journal
Science (New York, N.Y.)
Abbr.
Science
ISSN
0036-8075
Published
1988-04-08
Pages
196-9
Language
English
Region
United States
NLM ID
0404511
Subset
IM
Grants
NCI NIH HHS · CA34610 · United States
NCI NIH HHS · CA39826 · United States
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