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J. Biol. Chem., Vol. 269, Issue 42, 26449-26455, Oct, 1994
L Sun, G Wu, JK Willson, E Zborowska, J Yang, I Rajkarunanayake, J Wang, LE Gentry, XF Wang and MG Brattain
The role of transforming growth factor (TGF) beta type II receptor in
reversing the malignant phenotype of human breast cancer MCF-7 cells was
examined. MCF-7 cells were insensitive to TGF beta 1 and expressed
undetectable levels of cell surface TGF beta type I receptor (RI) and type
II receptor (RII) by cross-linking with 125I-TGF beta 1. Stable
transfection of a RII expression vector yielded 3 transfectants with
varying levels of exogenous RII mRNA and protein levels. Expression of RII
also increased TGF beta 1 binding to RI in all 3 clones. Proliferation of
RII-positive clones was inhibited by exogenous TGF beta 1 in a
dose-dependent manner, whereas the control clones remained TGF
beta-insensitive. The RII transfectants were growth arrested in monolayer
culture at saturation densities which were 41-66% of that of the Neo
controls. They also showed reduced clonogenicity in soft- agarose.
Tumorigenicity in ovariectomized, estrogen-supplemented nude mice was
delayed in transfectants with low RII levels. Transfectants expressing high
levels of RII showed a large reduction in tumorigenicity as well as a
longer delay in tumor formation. Tumor growth was associated with loss of
exogenous RII expression in transfectants. The results indicate that when
systems for TGF beta signal transduction are intact, reconstitution of the
TGF beta receptor system can lead to reversion of malignancy in cells
lacking RII.
Expression of transforming growth factor beta type II receptor leads to reduced malignancy in human breast cancer MCF-7 cells
Medical College of Ohio, Department of Biochemistry and Molecular Biology, Toledo 43614.
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