Feedback inhibition of Akt signaling limits the growth of tumors lacking Tsc2 Academic Article uri icon

Overview

MeSH Major

  • Cell Division
  • Feedback
  • Protein-Serine-Threonine Kinases
  • Proto-Oncogene Proteins
  • Repressor Proteins
  • Signal Transduction
  • Tumor Suppressor Proteins

abstract

  • The PTEN and TSC2 tumor suppressors inhibit mammalian target of rapamycin (mTOR) signaling and are defective in distinct hamartoma syndromes. Using mouse genetics, we find that Pten and Tsc2 act synergistically to suppress the severity of a subset of tumors specific to loss of each of these genes. Interestingly, we find that the slow-growing tumors specific to Tsc2+/- mice exhibit defects in signaling downstream of Akt. However, Pten haploinsufficiency restores Akt signaling in these tumors and dramatically enhances their severity. This study demonstrates that attenuation of the PI3K-Akt pathway in tumors lacking TSC2 contributes to their benign nature.

publication date

  • August 2005

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC1182339

Digital Object Identifier (DOI)

  • 10.1101/gad.1314605

PubMed ID

  • 16027169

Additional Document Info

start page

  • 1773

end page

  • 8

volume

  • 19

number

  • 15