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Updated: Apr 18, 2026

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
Targeting mitochondria in triple-negative breast cancer: Emerging therapeutic and drug development strategies
Ziyue Yuan1, Dan Mu1, Xiya Chen2
1Sichuan Engineering Research Center for Biomimetic Synthesis of Natural Drugs, School of Life Science and Engineering, Southwest Jiaotong University, Chengdu 610031, China.
Abstract:
Mitochondria are essential regulators of cell metabolism, apoptosis, and oxidative stress, rendering them critical targets for cancer therapy. This review systematically dissects the multifaceted roles of mitochondrial dysfunction in triple-negative breast cancer (TNBC), including its contributions to tumor initiation, progression, metabolic reprogramming, immune evasion, and programmed cell death, as well as its communication with other organelles. We summarize the current landscape of mitochondria-targeted therapeutic strategies for TNBC, encompassing direct targeting of mitochondrial proteins, indirect modulation of mitochondrial function via signaling pathways, mitochondria-targeted modification, and drug combination regimens. Additionally, we examine emerging approaches such as nanoparticle delivery systems and clinical compounds with mitochondrial regulatory effects. This review aims to provide a comprehensive framework for advancing the development of more precise and effective mitochondria-targeted therapies against TNBC.
Insights
Mitochondrial dysfunction fuels triple-negative breast cancer (TNBC) growth and spread. This review explores new therapies targeting mitochondria to combat TNBC, offering hope for more effective treatments.
Area of Science:
- Mitochondrial biology and cancer therapeutics
Background:
- Mitochondria regulate critical cellular processes like metabolism and apoptosis.
- Mitochondrial dysfunction is increasingly recognized as a key driver in triple-negative breast cancer (TNBC).
Purpose of the Study:
- To systematically review the roles of mitochondrial dysfunction in TNBC.
- To summarize current and emerging mitochondria-targeted therapeutic strategies for TNBC.
Main Methods:
- Comprehensive literature review of mitochondrial dysfunction in TNBC.
- Analysis of therapeutic strategies targeting mitochondria in TNBC, including direct and indirect approaches.
- Examination of novel delivery systems and compounds.
Main Results:
- Mitochondrial dysfunction contributes to TNBC initiation, progression, metabolic reprogramming, immune evasion, and cell death.
- Current therapies include direct mitochondrial protein targeting, pathway modulation, and combination regimens.
- Emerging strategies involve nanoparticles and compounds with mitochondrial regulatory effects.
Conclusions:
- Targeting mitochondria offers a promising avenue for developing precise and effective TNBC therapies.
- Further research into mitochondria-targeted approaches is crucial for advancing TNBC treatment.
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