Loss of TGF-β signaling in epithelial-derived tumors: Mechanisms and biological consequences

James W Freeman

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

The purpose of this article is to review current knowledge of the role that loss in transforming growth factor beta (TGF-β) signaling has on the tumorgenicity of epithelial derived tumors. The mechanisms responsible for loss in TGF-β signaling are also summarized. Loss in response to TGF-β is one of the hallmarks of tumor progression. Loss in TGF-β signaling provides cells with a selective growth advantage by diminishing the expression of cyclin-dependent kinase inhibitors, circumventing cell cycle checkpoints, and promoting cell survival The loss of TGF-β signaling is mediated by a variety of mechanisms. These include mutations that inactivate TGF-β receptors and Smads, expression of oncoproteins ski and sno that inactivate Smad complexes, over-expression of antagonistic Smads, and epigenetic events that down regulate TGF-β receptor expression. A further understanding of these mechanisms may lead to the development of therapeutic strategies that restore TGF-β signaling.

Original languageEnglish (US)
Pages (from-to)239-244
Number of pages6
JournalJournal of Clinical Ligand Assay
Volume23
Issue number3
StatePublished - 2000

Fingerprint

Transforming Growth Factor beta
Tumors
Transforming Growth Factor beta Receptors
Neoplasms
Cells
Cell signaling
Cyclin-Dependent Kinases
Oncogene Proteins
Cell Cycle Checkpoints
Epigenomics
Cell Survival
Down-Regulation
Mutation
Growth

Keywords

  • Cancer
  • Cell cycle
  • Gene regulation
  • Growth regulation
  • Smads
  • TGF-β
  • TGF-β receptors
  • Tumorigenicity

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Immunology

Cite this

Loss of TGF-β signaling in epithelial-derived tumors : Mechanisms and biological consequences. / Freeman, James W.

In: Journal of Clinical Ligand Assay, Vol. 23, No. 3, 2000, p. 239-244.

Research output: Contribution to journalArticle

@article{9187a86efd314821a2b300dc14697f08,
title = "Loss of TGF-β signaling in epithelial-derived tumors: Mechanisms and biological consequences",
abstract = "The purpose of this article is to review current knowledge of the role that loss in transforming growth factor beta (TGF-β) signaling has on the tumorgenicity of epithelial derived tumors. The mechanisms responsible for loss in TGF-β signaling are also summarized. Loss in response to TGF-β is one of the hallmarks of tumor progression. Loss in TGF-β signaling provides cells with a selective growth advantage by diminishing the expression of cyclin-dependent kinase inhibitors, circumventing cell cycle checkpoints, and promoting cell survival The loss of TGF-β signaling is mediated by a variety of mechanisms. These include mutations that inactivate TGF-β receptors and Smads, expression of oncoproteins ski and sno that inactivate Smad complexes, over-expression of antagonistic Smads, and epigenetic events that down regulate TGF-β receptor expression. A further understanding of these mechanisms may lead to the development of therapeutic strategies that restore TGF-β signaling.",
keywords = "Cancer, Cell cycle, Gene regulation, Growth regulation, Smads, TGF-β, TGF-β receptors, Tumorigenicity",
author = "Freeman, {James W}",
year = "2000",
language = "English (US)",
volume = "23",
pages = "239--244",
journal = "Journal of Clinical Ligand Assay",
issn = "1081-1672",
publisher = "Clinical Ligand Assay Society Inc.",
number = "3",

}

TY - JOUR

T1 - Loss of TGF-β signaling in epithelial-derived tumors

T2 - Mechanisms and biological consequences

AU - Freeman, James W

PY - 2000

Y1 - 2000

N2 - The purpose of this article is to review current knowledge of the role that loss in transforming growth factor beta (TGF-β) signaling has on the tumorgenicity of epithelial derived tumors. The mechanisms responsible for loss in TGF-β signaling are also summarized. Loss in response to TGF-β is one of the hallmarks of tumor progression. Loss in TGF-β signaling provides cells with a selective growth advantage by diminishing the expression of cyclin-dependent kinase inhibitors, circumventing cell cycle checkpoints, and promoting cell survival The loss of TGF-β signaling is mediated by a variety of mechanisms. These include mutations that inactivate TGF-β receptors and Smads, expression of oncoproteins ski and sno that inactivate Smad complexes, over-expression of antagonistic Smads, and epigenetic events that down regulate TGF-β receptor expression. A further understanding of these mechanisms may lead to the development of therapeutic strategies that restore TGF-β signaling.

AB - The purpose of this article is to review current knowledge of the role that loss in transforming growth factor beta (TGF-β) signaling has on the tumorgenicity of epithelial derived tumors. The mechanisms responsible for loss in TGF-β signaling are also summarized. Loss in response to TGF-β is one of the hallmarks of tumor progression. Loss in TGF-β signaling provides cells with a selective growth advantage by diminishing the expression of cyclin-dependent kinase inhibitors, circumventing cell cycle checkpoints, and promoting cell survival The loss of TGF-β signaling is mediated by a variety of mechanisms. These include mutations that inactivate TGF-β receptors and Smads, expression of oncoproteins ski and sno that inactivate Smad complexes, over-expression of antagonistic Smads, and epigenetic events that down regulate TGF-β receptor expression. A further understanding of these mechanisms may lead to the development of therapeutic strategies that restore TGF-β signaling.

KW - Cancer

KW - Cell cycle

KW - Gene regulation

KW - Growth regulation

KW - Smads

KW - TGF-β

KW - TGF-β receptors

KW - Tumorigenicity

UR - http://www.scopus.com/inward/record.url?scp=0034491244&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034491244&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:0034491244

VL - 23

SP - 239

EP - 244

JO - Journal of Clinical Ligand Assay

JF - Journal of Clinical Ligand Assay

SN - 1081-1672

IS - 3

ER -