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Updated: Feb 2, 2026

Evaluating the Role of Mitochondrial Function in Cancer-related Fatigue
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The Role of PI3K in Met Driven Cancer: A Recap

Alexia Hervieu1,2, Stéphanie Kermorgant2

  • 1Signal Transduction and Molecular Pharmacology Team, Cancer Therapeutics Division, Institute of Cancer Research, Sutton, United Kingdom.

Frontiers in Molecular Biosciences
|November 9, 2018
PubMed

Insights

Met receptor tyrosine kinase (RTK) signaling is crucial in cancer. Targeting downstream Phosphatidylinositide 3-kinase (PI3K)/Akt/mTOR pathways offers new therapeutic strategies against Met-driven cancers and resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signaling Pathways

Background:

  • The Met receptor tyrosine kinase (RTK) is frequently altered in cancer, driving tumor progression.
  • Met signaling activates crucial downstream pathways, including Phosphatidylinositide 3-kinase (PI3K).
  • Drug resistance to RTK inhibitors necessitates targeting downstream effectors like PI3K/Akt/mTOR.

Purpose of the Study:

  • To review the activation and role of the PI3K/Akt/mTOR pathway downstream of Met in cancer.
  • To highlight the significance of these pathways in Met-driven oncogenesis.
  • To discuss the implications for developing novel cancer therapies.

Main Methods:

  • Literature review of preclinical and clinical studies.
  • Analysis of molecular mechanisms of Met signaling.
  • Examination of PI3K/Akt/mTOR pathway components and their functions.

Main Results:

  • Met receptor activation leads to the deregulation of the PI3K/Akt/mTOR pathway.
  • This pathway controls key cellular processes including proliferation, survival, and metabolism.
  • Understanding these interactions is vital for therapeutic intervention.

Conclusions:

  • The PI3K/Akt/mTOR pathway is a critical mediator of Met-driven cancer.
  • Targeting this pathway offers a promising strategy to overcome resistance to Met inhibitors.
  • Further research into these molecular players can lead to improved cancer treatments.
Keywords:
AktMetPI3KcancermTORsignaling

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