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PI3K/AKT pathway as a key link modulates the multidrug resistance of cancers

Rui Liu1, Youwen Chen1, Guangzhi Liu1

  • 1School of Chinese Materia Medica, Beijing University of Chinese Medicine, 100029, Beijing, China.

Cell Death & Disease
|September 25, 2020
PubMed

Insights

Multidrug resistance (MDR) in cancer is often driven by aberrant activation of the Phosphatidylinositol 3-kinase (PI3K)/Protein kinase B (AKT) pathway. Understanding this link is crucial for overcoming chemotherapy failure.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Multidrug resistance (MDR) is a primary cause of chemotherapy failure in cancer treatment.
  • The Phosphatidylinositol 3-kinase (PI3K) pathway plays a critical role in cellular signaling and is implicated in chemoresistance.
  • Protein kinase B (AKT), a downstream effector of PI3K, regulates key processes like apoptosis, cell growth, and metabolism.

Purpose of the Study:

  • To review the role of aberrant PI3K/AKT pathway activation in modulating MDR.
  • To summarize key targets regulated by the PI3K/AKT pathway that are associated with MDR.

Main Methods:

  • Literature review focusing on the PI3K/AKT pathway and its relation to cancer multidrug resistance.
  • Analysis of molecular mechanisms linking PI3K/AKT signaling to chemoresistance.

Main Results:

  • Aberrant PI3K/AKT activation is a central mechanism contributing to MDR in various cancers.
  • The pathway influences MDR through regulation of apoptosis-related proteins, ABC transporters, GSK-3β, NF-κB, mTOR, and glycolysis.

Conclusions:

  • Targeting the PI3K/AKT pathway presents a promising strategy to overcome MDR and improve cancer chemotherapy efficacy.
  • Further research into the specific molecular targets within this pathway could lead to novel therapeutic interventions.

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