A twist for survival and cancer progression

Br J Cancer. 2006 Jan 16;94(1):13-7. doi: 10.1038/sj.bjc.6602876.


A major obstacle to the expansion of abnormal cells with significant proliferative potential is the induction of programmed cell death. Consequently, oncogene-driven hyperproliferation must be associated with apoptosis inhibition to allow malignant outgrowth. The oncogenic cooperation of N-Myc and Twist-1 in the development of neuroblastoma, the most common and deadly solid tumour of childhood, perfectly illustrates such a process. N-Myc promotes cell proliferation, whereas Twist-1 counteracts its pro-apoptotic properties by knocking-down the ARF/p53 pathway. On the basis of numerous recent studies reporting its overexpression in a variety of human cancers, we discuss in this review the role of Twist-1 as a potent inhibitor of the cell safety programs engaged in response to an abnormal mitogenic activity.

Publication types

  • Review

MeSH terms

  • Apoptosis*
  • Breast Neoplasms / physiopathology*
  • Cell Proliferation
  • Disease Progression
  • Humans
  • Neoplasm Metastasis
  • Neuroblastoma / physiopathology*
  • Nuclear Proteins
  • Proto-Oncogene Proteins c-myc / physiology
  • Survival
  • Twist-Related Protein 1


  • Nuclear Proteins
  • Proto-Oncogene Proteins c-myc
  • TWIST1 protein, human
  • Twist-Related Protein 1