Mechanisms in TGF-beta action.

J. Massagué, J. Heino, M. Laiho

Research output: Contribution to journalArticlepeer-review

Abstract

The various isoforms of TGF-beta are multifunctional. We are exploring pathways of cellular regulation by TGF-beta that lead to suppression of cell proliferation, modulation of cell adhesion and control of cell differentiation. These cellular responses appear to be activated by binding of TGF-beta to a similar set of receptor glycoproteins in all cell types. TGF-beta receptor types I and II are specifically lost in cell mutants that are resistant to TGF-beta. The concomitant loss of these two receptors in certain mutants suggests that they are components of the TGF-beta signal-transducing receptor complex. Inhibition of epithelial cell proliferation by TGF-beta is linked to retention of the retinoblastoma growth suppressor gene product in an underphosphorylated state that is presumed to have growth suppressive activity. Inhibition of myogenic differentiation by TGF-beta involves a block in the expression of the master myogenic differentiation genes, such as myogenin, but appears also to involve up-regulation of extracellular matrix production. Expression of components of the cell adhesion apparatus--cell adhesion receptors and extracellular matrix proteins--is controlled by TGF-beta in an array of cell types. This response could have a great impact on the ability of cells to migrate, home to specific tissue locations and differentiate during development, invasion and metastasis.

Original languageEnglish (US)
Pages (from-to)51-59; discussion 59-5965
JournalCiba Foundation symposium
Volume157
StatePublished - 1991
Externally publishedYes

ASJC Scopus subject areas

  • General

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