Growth inhibition by transforming growth factor β (TGF-β) type I is restored in TGF-β-resistant hepatoma cells after expression of TGF-β receptor type II cDNA

Mitsuhiro Inagaki; Aristidis Moustakas; Herbert Y. Lin; Harvey F. Lodish; Brian I. Carr

Growth inhibition by transforming growth factor β (TGF-β) type I is restored in TGF-β-resistant hepatoma cells after expression of TGF-β receptor type II cDNA

Mitsuhiro Inagaki, Aristidis Moustakas, Herbert Y. Lin, Harvey F. Lodish, Brian I. Carr

Ente Ospedaliero Specializzato in Gastroenterologia "Saverio de Bellis"

Research output: Contribution to journal › Article › peer-review

Abstract

The growth of human hepatoma Hep 3B cells is potently inhibited by TGF-β₁, (ID₅₀ = 0.2 ng/ml, 8 pM). A mutant cell line was derived that was not inhibited in growth by TGF-β₁ at 5 ng/ml (200 pM) and that lacked TGF-β receptor type II (TGF-βRII) gene. Transfection of the cloned cDNA for human TGF-βRII to this mutant cell line restored receptor expression as well as the inhibition in growth by TGF-β₁. In both wild-type and mutant cells stably transfected with TGF-βRII cDNA, TGF-βRII coimmunoprecipitated with TGF-β receptor type I in the presence of ligand. These experiments provide direct evidence for the role of TGF-βRII in the inhibitory effect of TGF-β on growth and suggest that TGF-βRII acts by means of a heteromeric surface complex with TGF-β receptor type I.

Original language	English
Pages (from-to)	5359-5363
Number of pages	5
Journal	Proceedings of the National Academy of Sciences of the United States of America
Volume	90
Issue number	11
Publication status	Published - Jun 1 1993

Keywords

Human hepatoma
Polyclonal antisera
Transfection

ASJC Scopus subject areas

General
Genetics

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Growth inhibition by transforming growth factor β (TGF-β) type I is restored in TGF-β-resistant hepatoma cells after expression of TGF-β receptor type II cDNA. / Inagaki, Mitsuhiro; Moustakas, Aristidis; Lin, Herbert Y. et al.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 90, No. 11, 01.06.1993, p. 5359-5363.

Research output: Contribution to journal › Article › peer-review

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title = "Growth inhibition by transforming growth factor β (TGF-β) type I is restored in TGF-β-resistant hepatoma cells after expression of TGF-β receptor type II cDNA",

abstract = "The growth of human hepatoma Hep 3B cells is potently inhibited by TGF-β1, (ID50 = 0.2 ng/ml, 8 pM). A mutant cell line was derived that was not inhibited in growth by TGF-β1 at 5 ng/ml (200 pM) and that lacked TGF-β receptor type II (TGF-βRII) gene. Transfection of the cloned cDNA for human TGF-βRII to this mutant cell line restored receptor expression as well as the inhibition in growth by TGF-β1. In both wild-type and mutant cells stably transfected with TGF-βRII cDNA, TGF-βRII coimmunoprecipitated with TGF-β receptor type I in the presence of ligand. These experiments provide direct evidence for the role of TGF-βRII in the inhibitory effect of TGF-β on growth and suggest that TGF-βRII acts by means of a heteromeric surface complex with TGF-β receptor type I.",

keywords = "Human hepatoma, Polyclonal antisera, Transfection",

author = "Mitsuhiro Inagaki and Aristidis Moustakas and Lin, {Herbert Y.} and Lodish, {Harvey F.} and Carr, {Brian I.}",

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T1 - Growth inhibition by transforming growth factor β (TGF-β) type I is restored in TGF-β-resistant hepatoma cells after expression of TGF-β receptor type II cDNA

AU - Inagaki, Mitsuhiro

AU - Moustakas, Aristidis

AU - Lin, Herbert Y.

AU - Lodish, Harvey F.

AU - Carr, Brian I.

PY - 1993/6/1

Y1 - 1993/6/1

N2 - The growth of human hepatoma Hep 3B cells is potently inhibited by TGF-β1, (ID50 = 0.2 ng/ml, 8 pM). A mutant cell line was derived that was not inhibited in growth by TGF-β1 at 5 ng/ml (200 pM) and that lacked TGF-β receptor type II (TGF-βRII) gene. Transfection of the cloned cDNA for human TGF-βRII to this mutant cell line restored receptor expression as well as the inhibition in growth by TGF-β1. In both wild-type and mutant cells stably transfected with TGF-βRII cDNA, TGF-βRII coimmunoprecipitated with TGF-β receptor type I in the presence of ligand. These experiments provide direct evidence for the role of TGF-βRII in the inhibitory effect of TGF-β on growth and suggest that TGF-βRII acts by means of a heteromeric surface complex with TGF-β receptor type I.

AB - The growth of human hepatoma Hep 3B cells is potently inhibited by TGF-β1, (ID50 = 0.2 ng/ml, 8 pM). A mutant cell line was derived that was not inhibited in growth by TGF-β1 at 5 ng/ml (200 pM) and that lacked TGF-β receptor type II (TGF-βRII) gene. Transfection of the cloned cDNA for human TGF-βRII to this mutant cell line restored receptor expression as well as the inhibition in growth by TGF-β1. In both wild-type and mutant cells stably transfected with TGF-βRII cDNA, TGF-βRII coimmunoprecipitated with TGF-β receptor type I in the presence of ligand. These experiments provide direct evidence for the role of TGF-βRII in the inhibitory effect of TGF-β on growth and suggest that TGF-βRII acts by means of a heteromeric surface complex with TGF-β receptor type I.

KW - Human hepatoma

KW - Polyclonal antisera

KW - Transfection

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JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

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ER -

Growth inhibition by transforming growth factor β (TGF-β) type I is restored in TGF-β-resistant hepatoma cells after expression of TGF-β receptor type II cDNA

Abstract

Keywords

ASJC Scopus subject areas

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