AKT and cancer--is it all mTOR?

Cancer Cell. 2006 Oct;10(4):254-6. doi: 10.1016/j.ccr.2006.10.001.

Abstract

AKT, a key regulator of cell proliferation and survival, is commonly dysregulated in human cancers. Activated AKT kinase is oncogenic and required for tumorigenesis in PTEN-deficient animals. However, the importance of AKT in mediating transformation by other oncogenes and which of its targets are necessary for this process are poorly understood. In this issue of Cancer Cell, Skeen et al. show that AKT is required for transformation by mutant H-Ras and for experimental skin carcinogenesis. Moreover, the effects of AKT are mediated predominantly or solely via mTORC1. This suggests that AKT or mTOR inhibitors will be useful treatments for many cancers.

Publication types

  • Comment

MeSH terms

  • Animals
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Neoplasms / etiology*
  • Neoplasms / pathology
  • Protein Kinases / genetics
  • Protein Kinases / metabolism*
  • Proto-Oncogene Proteins c-akt / deficiency*
  • Proto-Oncogene Proteins c-akt / genetics
  • TOR Serine-Threonine Kinases

Substances

  • Protein Kinases
  • MTOR protein, human
  • TOR Serine-Threonine Kinases
  • mTOR protein, mouse
  • Proto-Oncogene Proteins c-akt