Related Experiment Video
Updated: Oct 25, 2025

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
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.
Abstract:
Triple-negative breast cancer (TNBC) is not as prevalent as hormone receptor or HER2-positive breast cancers and all receptor tests come back negative. More importantly, the heterogeneity and complexity of the TNBC on the molecular and clinical levels have limited the successful development of novel therapeutic strategies and led to intrinsic or developed resistance to chemotherapies and new therapeutic agents. Studies have demonstrated deregulation of Wnt/β-catenin signaling in tumorigenesis which plays decisive roles at the low survival rate of patients and facilitates resistance to currently existing therapies. This review summarizes mechanisms of Wnt/β-catenin signaling for resistance development in TNBC, the complex interaction between Wnt/β-catenin signaling, and the transactivated receptor tyrosine kinase (RTK) signaling pathways, lymphocytic infiltration, epithelial-mesenchymal transition (EMT), and induction of metastasis. Such associations and how these pathways interact in the development and progression of cancer have led to the careful analysis and development of new and effective combination therapies without generating significant toxicity and resistance.
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.
Related Concept Videos
Non-Canonical Wnt Signaling Pathways
Canonical Wnt Signaling Pathway
Treatment Resistant Cancers
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Targeted Cancer Therapies
There are several types of targeted therapies against...

