AKT in thyroid tumorigenesis and progression

Endocrinology. 2007 Mar;148(3):942-7. doi: 10.1210/en.2006-0937. Epub 2006 Aug 31.

Abstract

AKT (protein kinase B) is a central signaling molecule in the phosphatidyl inositol 3-kinase pathway that is frequently activated in human cancer. AKT activation regulates energy metabolism, apoptosis, proliferation, and migration in many cell systems. In thyroid cancer, AKT activation is involved in tumorigenesis, particularly in both inherited and sporadic forms of follicular thyroid cancer. Phosphatidyl inositol 3-kinase and AKT signaling also appear to play an important role in progression of both papillary and follicular cancers. In this review, the role of AKT in thyroid cancer development and progression are discussed with a focus on areas of current debate in the literature.

Publication types

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

MeSH terms

  • Animals
  • Carcinoma, Papillary / etiology*
  • Carcinoma, Papillary / metabolism
  • Carcinoma, Papillary, Follicular / etiology
  • Carcinoma, Papillary, Follicular / metabolism
  • Disease Progression
  • Humans
  • Models, Biological
  • Oncogene Protein v-akt / metabolism
  • Oncogene Protein v-akt / physiology*
  • Signal Transduction
  • Thyroid Neoplasms / etiology*
  • Thyroid Neoplasms / metabolism

Substances

  • Oncogene Protein v-akt