The PI3K/AKT signaling networks in cancer glucose metabolism: mechanisms and therapeutic implications

Sufen Cheng1, Qi Jiang2, Hua Huang1

  • 1Department of Hematology, The First Affiliated Hospital, Zhejiang University School of Medicine, Qingchun Road 79#, Hangzhou, Zhejiang Province 310003, China.

Insights

The PI3K/AKT pathway regulates cancer glucose metabolism. This review details its mechanisms, interactions with metabolic enzymes, and therapeutic targets for novel cancer treatments.

Area of Science:

  • Oncology
  • Molecular Biology
  • Metabolic Research

Background:

  • The Phosphatidylinositol 3-kinase/Protein Kinase B (PI3K/AKT) signaling pathway is a key regulator of cellular metabolism.
  • Dysregulation of the PI3K/AKT axis is a common event in cancer, significantly impacting glucose metabolism.
  • Understanding these metabolic alterations is crucial for developing effective cancer therapies.

Purpose of the Study:

  • To review the composition and activation mechanisms of the PI3K/AKT pathway.
  • To explore the interactions between PI3K/AKT, core metabolic enzymes, and their non-canonical roles in cancer.
  • To dissect the crosstalk between PI3K/AKT, AMP-activated protein kinase (AMPK), and major metabolic pathways.

Main Methods:

  • Literature review of the PI3K/AKT pathway in cancer metabolism.
  • Analysis of interactions between signaling pathways and metabolic enzymes.
  • Summary of current therapeutic strategies and challenges.

Main Results:

  • The PI3K/AKT pathway extensively influences core metabolic enzymes like hexokinase and lactate dehydrogenase.
  • Significant crosstalk exists between PI3K/AKT, AMPK, and pathways such as the pentose phosphate pathway and oxidative phosphorylation.
  • Non-canonical roles of metabolic enzymes are implicated in cancer progression.

Conclusions:

  • The PI3K/AKT pathway is central to cancer metabolic reprogramming.
  • Targeting metabolic enzymes and combined therapies show promise for cancer treatment.
  • Further research into PI3K/AKT-mediated metabolic reprogramming is needed to identify novel therapeutic targets.

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