Triple-negative breast cancer: understanding Wnt signaling in drug resistance

Parnaz Merikhian1, Mohammad Reza Eisavand1, Leila Farahmand2

  • 1Recombinant protein department, Breast Cancer Research Center, Motamed Cancer Institute, ACECR, 146, South Gandhi Ave., Vanak Circus, Tehran, Iran.

Insights

Triple-negative breast cancer (TNBC) exhibits resistance to therapies due to Wnt/β-catenin signaling. Understanding its interaction with other pathways is key to developing effective combination treatments.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Triple-negative breast cancer (TNBC) is a heterogeneous cancer subtype lacking targeted therapies.
  • TNBC is associated with poor patient survival and resistance to existing treatments.
  • Wnt/β-catenin signaling is frequently deregulated in TNBC, contributing to therapeutic resistance.

Purpose of the Study:

  • To review the mechanisms of Wnt/β-catenin signaling in TNBC resistance.
  • To explore the interactions between Wnt/β-catenin signaling and other cancer-promoting pathways.
  • To inform the development of novel combination therapies for TNBC.

Main Methods:

  • Literature review of studies on Wnt/β-catenin signaling in TNBC.
  • Analysis of molecular and clinical data related to TNBC progression.
  • Examination of pathway crosstalk in cancer development and resistance.

Main Results:

  • Wnt/β-catenin signaling promotes TNBC resistance through various mechanisms.
  • Interactions with receptor tyrosine kinase (RTK) pathways, EMT, and metastasis are critical.
  • Lymphocytic infiltration is influenced by Wnt/β-catenin signaling in TNBC.

Conclusions:

  • Targeting Wnt/β-catenin signaling offers potential for overcoming TNBC resistance.
  • Combination therapies involving Wnt/β-catenin modulators may improve outcomes.
  • Further research into pathway interactions is crucial for effective TNBC treatment strategies.

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