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Updated: Aug 15, 2026

Preparation of Mitochondria from Ovarian Cancer Tissues and Control Ovarian Tissues for Quantitative Proteomics Analysis
Published on: November 18, 2019
Senescence-associated mitochondrial dysfunction as a therapeutic target in ovarian cancer: Challenges and
Hanieh Sadat Khalili1, Banafshe Abadi2, Nima Rezaei3
1Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
None:
Senescence-associated mitochondrial dysfunction (SAMD) links aging, metabolic reprogramming, and therapy resistance in ovarian cancer. Persistent damage to mitochondrial DNA (mtDNA), impaired mitochondrial quality control, and disrupted mitochondrial fusion and fission dynamics compromise electron transport (ET) and membrane potential, yielding chronic mitochondrial reactive oxygen species. This, in turn, drives a senescence-associated secretory phenotype, which includes proinflammatory cytokines, matrix proteases, and pro-angiogenic factors. This secretory phenotype alters the tumor microenvironment in ways that make the cells more resistant to cell death. In this review, we provide comprehensive insights from preclinical and translational clinical studies to map mechanistic connections and outline pragmatic measurement strategies. Our goal is to explore whether SAMD can move from being merely a descriptive hallmark to a measurable biomarker and a practical therapeutic target for restoring chemosensitivity.
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