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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.
Abstract:
Triple-negative breast cancer (TNBC) is an aggressive and highly metastatic form of breast cancer and is associated with poor prognosis due to the lack of targeted therapies. Mitochondrial dysfunction is a crucial factor contributing to tumor growth and chemoresistance in TNBC. Dysregulation in mitochondrial dynamics leads to disruption of the normal process of oxidative phosphorylation, elevated reactive oxygen species generation, and resistance to apoptosis, contributing to TNBC aggressiveness. Moreover, alterations in mitochondrial energetics, including elevated glycolysis and glutamine addiction, provide metabolic advantages for TNBC growth and survival. Emerging therapeutic strategies targeting mitochondrial vulnerabilities have shown potential for TNBC management. Inhibitors targeting mitochondrial dynamics, including Mdivi-1, dynasore, and cepharanthine, act by restoring mitochondrial homeostasis and impairing excessive fission to stimulate apoptosis. Mitochondrial energetics inhibitors, such as 2DG, 3BP, clotrimazole, and etomoxir, disrupt mitochondrial metabolic processes and reduce tumor growth in TNBC. This review highlights the latest advancements in mitochondrial dynamics and energetics in TNBC and explores the molecular mechanisms underlying their dysregulation. It also explores the therapeutic potential of targeting mitochondrial function for personalized strategies leading to improved clinical management of TNBC.
Insights
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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