Akt isoform-specific signaling in breast cancer: uncovering an anti-migratory role for palladin

Cell Adh Migr. May-Jun 2011;5(3):211-4. doi: 10.4161/cam.5.3.15790. Epub 2011 May 1.


Numerous studies have shown that Akt isoforms promote tumorigenesis by enhancing cancer cell survival and growth, and it is well established that signaling through the Akt upstream regulator PI 3-K enhances cancer cell migration. Therefore, it is conventionally accepted that PI 3-K/Akt pathway promotes tumor formation and metastasis. A few years ago, studies from several laboratories added a new layer to the pleiotropic effects of Akt function by showing that the Akt1 isoform inhibits breast cancer cell migration and invasion, whereas Akt2 promotes these phenotypes. These studies challenged the dogma and identified non-redundant functions of Akt isoforms in cancer progression. The identification of palladin as an Akt1-specific substrate in our recently published work has exemplified distinct Akt isoform-specific signaling in breast cancer. Here, we review these findings and discuss the implications for the understanding of the mechanistic basis for designing more effective anti-cancer therapeutics targeting the Akt pathway.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Breast Neoplasms / metabolism*
  • Cytoskeletal Proteins / metabolism*
  • Female
  • Humans
  • Phosphoproteins / metabolism*
  • Protein Isoforms / metabolism*
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Signal Transduction / genetics
  • Signal Transduction / physiology*


  • Cytoskeletal Proteins
  • Phosphoproteins
  • Protein Isoforms
  • palladin protein, human
  • Proto-Oncogene Proteins c-akt