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PI3K/AKT/mTOR signaling pathway: an important driver and therapeutic target in triple-negative breast cancer

Huan-Ping Zhang1,2, Rui-Yuan Jiang1,3, Jia-Yu Zhu1,3

  • 1Zhejiang Cancer Hospital, Hangzhou Institute of Medicine (HIM), Chinese Academy of Sciences, Hangzhou, 310000, Zhejiang, China.

Breast Cancer (Tokyo, Japan)
|April 17, 2024
PubMed

Insights

Triple-negative breast cancer (TNBC) is aggressive and hard to treat. Targeting the PI3K/AKT/mTOR pathway offers a promising therapeutic strategy for TNBC, with ongoing clinical studies exploring kinase inhibitors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype lacking ER, PR, and HER2 expression, characterized by high metastasis and poor prognosis.
  • Limited effective therapeutic options exist for TNBC, necessitating novel treatment strategies.
  • The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) pathway is frequently over-activated in cancers, driving tumor growth and survival.

Purpose of the Study:

  • To review the activation mechanisms of the PI3K/AKT/mTOR pathway in TNBC.
  • To explore the relationship between PI3K/AKT/mTOR pathway activation and different TNBC subtypes.
  • To summarize recent clinical studies on kinase inhibitors targeting this pathway for TNBC treatment.

Main Methods:

  • Literature review of scientific articles and clinical trial data.
  • Analysis of PI3K/AKT/mTOR pathway activation mechanisms in TNBC.
  • Synthesis of findings from clinical studies on PI3K/AKT/mTOR inhibitors in TNBC.

Main Results:

  • The PI3K/AKT/mTOR pathway is a key driver in TNBC, contributing to its aggressive phenotype.
  • Specific activation patterns of this pathway correlate with different TNBC subtypes.
  • Kinase inhibitors targeting the PI3K/AKT/mTOR pathway show potential in treating TNBC, with several clinical studies underway.

Conclusions:

  • The PI3K/AKT/mTOR pathway represents a critical therapeutic target for TNBC.
  • Understanding pathway activation in specific TNBC subtypes can guide treatment selection.
  • Further research is needed to address challenges in the clinical application of these inhibitors for optimal TNBC management.
Keywords:
AKTPI3KPTENTargeted therapyTriple-negative breast cancer

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