Abstract
In Mv1Lu cells, insulin partially reverses transforming growth factor-beta1 (TGF-beta1) growth inhibition in the presence of alpha5beta1 integrin antagonists. TGF-beta1 appears to induce phosphorylation of IRS-2 in these cells; this is inhibited by a TGF-beta antagonist known to reverse TGF-beta growth inhibition. Stable transfection of 32D myeloid cells (which lack endogenous IRS proteins and are insensitive to growth inhibition by TGF-beta1) with IRS-1 or IRS-2 cDNA confers sensitivity to growth inhibition by TGF-beta1; this IRS-mediated growth inhibition can be partially reversed by insulin in 32D cells stably expressing IRS-2 and the insulin receptor (IR). These results suggest that growth inhibition by TGF-beta1 involves IRS proteins.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Cell Division
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Cell Line
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Cell Line, Tumor
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DNA / biosynthesis
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DNA / metabolism
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DNA, Complementary / metabolism
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Dose-Response Relationship, Drug
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Insulin / metabolism
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Insulin Receptor Substrate Proteins
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Integrin alpha5beta1 / antagonists & inhibitors
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Intracellular Signaling Peptides and Proteins
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Leukemia Virus, Murine
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Mice
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Phosphoproteins / metabolism
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Phosphorylation
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Precipitin Tests
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Protein Binding
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Receptor, Insulin / metabolism
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Signal Transduction
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Transfection
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Transforming Growth Factor beta / metabolism*
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Transforming Growth Factor beta1
Substances
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DNA, Complementary
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Insulin
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Insulin Receptor Substrate Proteins
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Integrin alpha5beta1
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Intracellular Signaling Peptides and Proteins
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Irs1 protein, mouse
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Irs2 protein, mouse
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Phosphoproteins
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Tgfb1 protein, mouse
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Transforming Growth Factor beta
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Transforming Growth Factor beta1
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DNA
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Receptor, Insulin