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Transmitochondrial Cybrid Generation Using Cancer Cell Lines
Published on: March 17, 2023
Mitochondrial dynamics: A promising tool for personalized TNBC management
Harshit Mishra1, Anshu Yadav1, Veena B Kushwaha1
1Department of Zoology, Deen Dayal Upadhyaya Gorakhpur University, Gorakhpur, Uttar Pradesh, 273009, India.
Genes & Diseases
|July 26, 2026
Summary
Triple-negative breast cancer (TNBC) is aggressive due to mitochondrial dysfunction. Targeting mitochondrial dynamics and energetics offers new therapeutic strategies for improved TNBC treatment and patient outcomes.
Area of Science:
- Oncology
- Molecular Biology
- Metabolic Research
Background:
- Triple-negative breast cancer (TNBC) is an aggressive subtype with poor prognosis due to limited targeted therapies.
- Mitochondrial dysfunction significantly contributes to TNBC growth, metastasis, and chemoresistance.
- Dysregulated mitochondrial dynamics and altered energetics provide metabolic advantages for TNBC survival.
Purpose of the Study:
- To review recent advancements in understanding mitochondrial dynamics and energetics in TNBC.
- To explore the molecular mechanisms behind mitochondrial dysregulation in TNBC.
- To discuss the therapeutic potential of targeting mitochondrial function for TNBC management.
Main Methods:
- Literature review of studies on mitochondrial dynamics and energetics in TNBC.
- Analysis of molecular mechanisms underlying mitochondrial dysfunction in TNBC.
- Evaluation of emerging therapeutic strategies targeting mitochondrial pathways.
Main Results:
- Mitochondrial dynamics inhibitors (e.g., Mdivi-1) restore homeostasis and induce apoptosis.
- Energetics inhibitors (e.g., 2DG) disrupt metabolic pathways, reducing TNBC growth.
- Targeting mitochondrial vulnerabilities presents promising avenues for TNBC treatment.
Conclusions:
- Mitochondrial dysfunction is a key driver of TNBC aggressiveness and chemoresistance.
- Targeting mitochondrial dynamics and energetics shows therapeutic potential for TNBC.
- Personalized strategies focused on mitochondrial function could improve TNBC clinical management.
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