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PI3K Signaling in Tissue Hyper-Proliferation: From Overgrowth Syndromes to Kidney Cysts

Maria Chiara De Santis1, Valentina Sala2, Miriam Martini3

  • 1Department of Molecular Biotechnology and Health Sciences, University of Torino, Torino 10126, Italy. mariachiara.desantis@unito.it.

Cancers
|March 30, 2017
PubMed

Insights

The Phosphoinositide-3 Kinase (PI3K)/AKT/mammalian Target Of Rapamycin (mTOR) pathway regulates cell proliferation. Alterations in this pathway drive diseases beyond cancer, including overgrowth disorders and polycystic kidney disease.

Area of Science:

  • Molecular Biology
  • Cell Signaling
  • Biochemistry

Background:

  • The Phosphoinositide-3 Kinase (PI3K) protein family regulates cell proliferation via lipid second messengers.
  • PI3K activates the AKT/PKB (AKT) and mammalian Target Of Rapamycin (mTOR) pathways.
  • While PI3K/AKT/mTOR pathway mutations are known in cancer, they also drive other diseases.

Purpose of the Study:

  • To review the PI3K/AKT/mTOR pathway's role in cell proliferation.
  • To compare PI3K alterations' effects across different tissues.
  • To discuss how pathway convergence leads to diverse biological outcomes.

Main Methods:

  • Literature review of PI3K/AKT/mTOR pathway research.
  • Comparative analysis of PI3K enzyme alterations in various tissues.
  • Synthesis of recent findings on signaling cascade interactions.

Main Results:

  • PI3K/AKT/mTOR pathway dysregulation contributes to diseases like overgrowth disorders and polycystic kidney disease.
  • The same pathway can yield different biological effects depending on tissue context.
  • Convergence and cooperation of signaling cascades modulate pathway outcomes.

Conclusions:

  • The PI3K/AKT/mTOR pathway is a critical regulator of cell proliferation with implications beyond cancer.
  • Understanding tissue-specific effects and signaling crosstalk is key to deciphering disease mechanisms.
  • Further research into PI3K pathway alterations can reveal novel therapeutic targets for various conditions.
Keywords:
PI3KmTORovergrowth syndromepolycystic kidney diseaseproliferation

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