c-Rel arrests the proliferation of HeLa cells and affects critical regulators of the G1/S-phase transition

Mol Cell Biol. 1997 Nov;17(11):6526-36. doi: 10.1128/MCB.17.11.6526.

Abstract

A tetracycline-regulated system was used to characterize the effects of c-Rel on cell proliferation. The expression of c-Rel in HeLa cells led to growth arrest at the G1/S-phase transition, which correlated with its nuclear localization and the induction of endogenous IkappaB alpha expression. These changes were accompanied by a decrease in E2F DNA binding and the accumulation of the hypophosphorylated form of Rb. In vitro kinase assays showed a reduction in Cdk2 kinase activity that correlated with elevated levels of p21WAF1 Cdk inhibitor and p53 tumor suppressor protein. While the steady-state levels of WAF1 transcripts were increased, pulse-chase analysis revealed a sharp increase in p53 protein stability. Importantly, the deletion of the C-terminal transactivation domains of c-Rel abolished these effects. Together, these studies demonstrate that c-Rel can affect cell cycle control and suggest the involvement of the p21WAF1 and p53 cell cycle regulators.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apoptosis / physiology
  • CDC2-CDC28 Kinases*
  • Carrier Proteins*
  • Cell Compartmentation
  • Cell Cycle / physiology*
  • Cell Cycle Proteins*
  • Cell Division / physiology
  • Cell Nucleus / metabolism
  • Chickens
  • Cyclin-Dependent Kinase 2
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclin-Dependent Kinases / metabolism
  • Cyclins / metabolism
  • DNA-Binding Proteins / biosynthesis
  • E2F Transcription Factors
  • G1 Phase / physiology
  • Gene Expression Regulation / drug effects
  • HeLa Cells
  • Humans
  • I-kappa B Proteins*
  • NF-KappaB Inhibitor alpha
  • Protein Binding
  • Protein Serine-Threonine Kinases / metabolism
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / metabolism*
  • Proto-Oncogene Proteins c-rel
  • Recombinant Proteins / metabolism
  • Retinoblastoma Protein / metabolism
  • Retinoblastoma-Binding Protein 1
  • S Phase / physiology
  • Tetracycline / pharmacology
  • Transcription Factor DP1
  • Transcription Factors / metabolism
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • CDKN1A protein, human
  • Carrier Proteins
  • Cell Cycle Proteins
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • DNA-Binding Proteins
  • E2F Transcription Factors
  • I-kappa B Proteins
  • NFKBIA protein, human
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-rel
  • Recombinant Proteins
  • Retinoblastoma Protein
  • Retinoblastoma-Binding Protein 1
  • Transcription Factor DP1
  • Transcription Factors
  • Tumor Suppressor Protein p53
  • NF-KappaB Inhibitor alpha
  • Protein Serine-Threonine Kinases
  • CDC2-CDC28 Kinases
  • CDK2 protein, human
  • Cyclin-Dependent Kinase 2
  • Cyclin-Dependent Kinases
  • Tetracycline