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PI3K and AKT: Unfaithful Partners in Cancer

Seraina Faes1, Olivier Dormond2

  • 1Department of Visceral Surgery, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Pavillon 4, Av. de Beaumont, Lausanne 1011, Switzerland. seraina.faes@chuv.ch.

International Journal of Molecular Sciences
|September 26, 2015
PubMed

Insights

The phosphatidylinositol 3-kinase (PI3K)/AKT pathway is crucial in cancer, but resistance limits PI3K/AKT inhibitors. Understanding PI3K and AKT

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • The phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway is integral to cellular functions.
  • Overactivation of this pathway is common in human cancers, driving tumor progression.
  • PI3K/AKT pathway inhibition is a key strategy in cancer therapy.

Purpose of the Study:

  • To elucidate the complex interplay between PI3K and AKT in cancer.
  • To discuss the therapeutic implications of this complex relationship.

Main Methods:

  • Review of current literature on PI3K/AKT signaling in cancer.
  • Analysis of resistance mechanisms to PI3K/AKT inhibitors.
  • Exploration of independent roles of PI3K and AKT in oncogenesis.

Main Results:

  • Resistance to PI3K/AKT inhibitors arises from feedback loop abrogation and alternative pathway activation.
  • Emerging evidence shows PI3K and AKT can function independently in cancer.
  • This independence adds complexity to targeting the PI3K/AKT pathway.

Conclusions:

  • The intricate relationship between PI3K and AKT presents challenges for effective cancer therapy.
  • Targeting strategies must account for the independent and cooperative roles of PI3K and AKT.
  • Further research is needed to overcome resistance and optimize PI3K/AKT-targeted treatments.
Keywords:
AKTPI3Kcancersignalingtherapies

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