Oncogenic cooperation between H-Twist and N-Myc overrides failsafe programs in cancer cells

Cancer Cell. 2004 Dec;6(6):625-30. doi: 10.1016/j.ccr.2004.09.033.

Abstract

N-Myc oncogene amplification is a frequent event in neuroblastoma and is strongly correlated with advanced disease stage and treatment failure. Similarly to c-Myc oncogenic activation, N-Myc deregulation promotes both cell proliferation and p53-dependent apoptosis by sensitizing cells to a variety of insults. Intriguingly, p53 mutations are uncommon in neuroblastomas, strongly suggesting that an alternative cooperating event circumvents this safeguard against oncogene-driven neoplasia. By performing a pangenomic cDNA microarray analysis, we demonstrate that human Twist is constantly overexpressed in N-Myc-amplified neuroblastomas. H-Twist overexpression is responsible for the inhibition of the ARF/p53 pathway involved in the Myc-dependent apoptotic response. This oncogenic cooperation of two key regulators of embryogenesis causes cell transformation and malignant outgrowth.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / physiology
  • Blotting, Northern
  • Blotting, Western
  • Caspase 3
  • Caspase 8
  • Caspases / metabolism
  • Cell Cycle Proteins / metabolism
  • Cell Line, Tumor
  • Cell Transformation, Neoplastic / genetics*
  • Cyclin-Dependent Kinase Inhibitor p16 / genetics
  • Cyclin-Dependent Kinase Inhibitor p21
  • Fibroblasts / pathology
  • Flow Cytometry
  • Gene Amplification
  • Gene Expression Regulation, Neoplastic / genetics
  • Humans
  • In Situ Nick-End Labeling
  • Mice
  • Neuroblastoma / genetics
  • Neuroblastoma / metabolism
  • Neuroblastoma / pathology*
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • Oligonucleotide Array Sequence Analysis
  • Proto-Oncogene Proteins c-myc / genetics
  • Proto-Oncogene Proteins c-myc / metabolism*
  • Proto-Oncogenes / genetics
  • RNA, Small Interfering / genetics
  • Reverse Transcriptase Polymerase Chain Reaction
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Transfection
  • Tumor Stem Cell Assay
  • Tumor Suppressor Protein p14ARF / genetics
  • Tumor Suppressor Protein p53 / metabolism
  • Twist-Related Protein 1

Substances

  • CDKN1A protein, human
  • Cdkn1a protein, mouse
  • Cell Cycle Proteins
  • Cyclin-Dependent Kinase Inhibitor p16
  • Cyclin-Dependent Kinase Inhibitor p21
  • Nuclear Proteins
  • Proto-Oncogene Proteins c-myc
  • RNA, Small Interfering
  • TWIST1 protein, human
  • Transcription Factors
  • Tumor Suppressor Protein p14ARF
  • Tumor Suppressor Protein p53
  • Twist-Related Protein 1
  • CASP3 protein, human
  • CASP8 protein, human
  • Casp3 protein, mouse
  • Casp8 protein, mouse
  • Caspase 3
  • Caspase 8
  • Caspases