TGF-beta 1 and cAMP attenuate cyclin A gene transcription via a cAMP responsive element through independent pathways

Oncogene. 1995 Oct 5;11(7):1309-18.

Abstract

Transforming growth factor beta (TGF-beta) is a potent inhibitor of the proliferation of many cell lines. The expression of Cyclin A is down-regulated by TGF-beta 1 in Chinese hamster lung fibroblasts and most of this effect is mediated at the transcriptional level through a cAMP-responsive element (CRE), but does not require a functional cAMP-dependent protein kinase. However, activation of the cAMP pathway in these cells gives rise to a strong inhibition of proliferation, paralleled by a down-regulation of Cyclin A promoter activity. This effect requires the integrity of the CRE, suggesting a role for CRE-binding proteins in late G1/S controls.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Cell Line
  • Cricetinae
  • Cricetulus
  • Cyclic AMP / physiology*
  • Cyclic AMP Response Element-Binding Protein / physiology*
  • Cyclins / genetics*
  • Cyclins / metabolism
  • DNA
  • Humans
  • Microinjections
  • Molecular Sequence Data
  • Promoter Regions, Genetic / physiology
  • Protein Binding
  • Regulatory Sequences, Nucleic Acid*
  • Transcription, Genetic*
  • Transforming Growth Factor beta / physiology*

Substances

  • Cyclic AMP Response Element-Binding Protein
  • Cyclins
  • Transforming Growth Factor beta
  • DNA
  • Cyclic AMP