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Published on: November 18, 2019
Targeting Mitochondrial Quality Control for the Treatment of Triple-Negative Breast Cancer: From Molecular Mechanisms
Wanjuan Pei1, Ling Dai1, Mingxiao Li1
1Medical College, Hunan University of Chinese Medicine, Changsha 410208, China.
Abstract:
Breast cancer is the leading threat to the health of women, with a rising global incidence linked to social and psychological factors. Among its subtypes, triple-negative breast cancer (TNBC), which lacks estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) expression, is highly heterogeneous with early metastasis and a poor prognosis, making it the most challenging subtype. Mounting evidence shows that the mitochondrial quality control (MQC) system is vital for maintaining cellular homeostasis. Dysfunction of the MQC is tied to tumor cell invasiveness, metastasis, and chemoresistance. This paper comprehensively reviews the molecular link between MQC and TNBC development. We focused on how abnormal MQC affects TNBC progression by influencing chemoresistance, immune evasion, metastasis, and cancer stemness. On the basis of current studies, new TNBC treatment strategies targeting key MQC nodes have been proposed. These findings increase the understanding of TNBC pathogenesis and offer a theoretical basis for overcoming treatment challenges, providing new research angles and intervention targets for effective precision therapy for TNBC.
Insights
Mitochondrial quality control (MQC) dysfunction promotes triple-negative breast cancer (TNBC) progression, affecting chemoresistance, metastasis, and stemness. Targeting MQC offers new precision therapy strategies for TNBC.
Area of Science:
- Oncology
- Cell Biology
- Molecular Medicine
Background:
- Triple-negative breast cancer (TNBC) is aggressive and lacks targeted therapies.
- Mitochondrial quality control (MQC) is crucial for cellular health and homeostasis.
- MQC dysfunction is implicated in cancer progression, including invasiveness and chemoresistance.
Purpose of the Study:
- To comprehensively review the molecular links between MQC and TNBC development.
- To explore how abnormal MQC influences TNBC progression, including chemoresistance, immune evasion, metastasis, and cancer stemness.
- To propose novel TNBC treatment strategies targeting key MQC nodes.
Main Methods:
- Literature review of current studies on MQC and TNBC.
- Analysis of molecular mechanisms connecting MQC dysfunction to TNBC characteristics.
- Synthesis of findings to propose new therapeutic targets.
Main Results:
- Abnormal MQC contributes to TNBC progression by affecting chemoresistance, immune evasion, metastasis, and cancer stemness.
- MQC dysfunction is a key factor in the heterogeneity and poor prognosis of TNBC.
- Specific MQC nodes represent potential targets for TNBC intervention.
Conclusions:
- Understanding the role of MQC in TNBC pathogenesis is critical for developing effective treatments.
- Targeting MQC pathways offers a promising avenue for precision therapy in TNBC.
- This review provides a theoretical basis for new research and intervention strategies against TNBC.
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