Mechanisms of suberoylanilide hydroxamic acid inhibition of mammary cell growth

Breast Cancer Res. 2001;3(2):122-33. doi: 10.1186/bcr284. Epub 2000 Dec 22.

Abstract

The mechanism of suberoylanilide hydroxamic acid in cell growth inhibition involved induction of pRb-2/p130 interaction and nuclear translocation with E2F-4, followed by significant repression in E2F-1 and PCNA nuclear levels, which led to inhibition in DNA synthesis in mammary epithelial cell lines.

Publication types

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

MeSH terms

  • Acetylation
  • Animals
  • Antineoplastic Agents / pharmacology*
  • Antineoplastic Agents / therapeutic use
  • Apoptosis / drug effects
  • Blotting, Western
  • Breast Neoplasms / drug therapy*
  • Carrier Proteins*
  • Cell Cycle / drug effects
  • Cell Cycle Proteins*
  • Cell Division / drug effects*
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclin-Dependent Kinases / metabolism
  • Cyclins / metabolism
  • DNA-Binding Proteins / metabolism
  • E2F Transcription Factors
  • E2F1 Transcription Factor
  • E2F4 Transcription Factor
  • Female
  • Flow Cytometry
  • Fluorescent Antibody Technique
  • Humans
  • Hydroxamic Acids / pharmacology*
  • Hydroxamic Acids / therapeutic use
  • Mice
  • Phosphorylation
  • Precipitin Tests
  • Proliferating Cell Nuclear Antigen / metabolism
  • Retinoblastoma-Binding Protein 1
  • Transcription Factor DP1
  • Transcription Factors / metabolism
  • Tumor Cells, Cultured / cytology
  • Tumor Cells, Cultured / drug effects
  • Up-Regulation / drug effects
  • Vorinostat

Substances

  • Antineoplastic Agents
  • Arid4a protein, mouse
  • CDKN1A protein, human
  • Carrier Proteins
  • Cdkn1a protein, mouse
  • Cell Cycle Proteins
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • DNA-Binding Proteins
  • E2F Transcription Factors
  • E2F1 Transcription Factor
  • E2F1 protein, human
  • E2F4 Transcription Factor
  • E2F4 protein, human
  • E2f1 protein, mouse
  • E2f4 protein, mouse
  • Hydroxamic Acids
  • Proliferating Cell Nuclear Antigen
  • Retinoblastoma-Binding Protein 1
  • Transcription Factor DP1
  • Transcription Factors
  • Vorinostat
  • Cyclin-Dependent Kinases