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Updated: Aug 15, 2026

Preparation of Mitochondria from Ovarian Cancer Tissues and Control Ovarian Tissues for Quantitative Proteomics Analysis
11:51

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.

European Journal of Pharmacology
|August 13, 2026
PubMed

Insights

Senescence-associated mitochondrial dysfunction (SAMD) drives ovarian cancer therapy resistance by altering the tumor microenvironment. Targeting SAMD may restore chemosensitivity and improve treatment outcomes.

Area of Science:

  • Oncology
  • Cellular Biology
  • Aging Research

Background:

  • Senescence-associated mitochondrial dysfunction (SAMD) is implicated in aging, metabolic changes, and therapy resistance in ovarian cancer.
  • Mitochondrial damage (mtDNA), impaired quality control, and altered dynamics lead to reactive oxygen species (ROS) and a senescence-associated secretory phenotype (SASP).
  • The SASP promotes a tumor microenvironment resistant to cell death, contributing to treatment failure.

Purpose of the Study:

  • To review preclinical and clinical evidence linking SAMD to ovarian cancer progression and therapy resistance.
  • To explore SAMD as a measurable biomarker for ovarian cancer.
  • To investigate SAMD as a therapeutic target for enhancing chemosensitivity.

Main Methods:

  • Comprehensive literature review of preclinical studies and translational clinical research.
  • Analysis of mechanistic connections between mitochondrial dysfunction and cancer hallmarks.
  • Evaluation of strategies for measuring SAMD in clinical settings.

Main Results:

  • SAMD contributes to metabolic reprogramming and therapy resistance in ovarian cancer.
  • Chronic mitochondrial ROS production drives a pro-tumorigenic SASP.
  • The altered tumor microenvironment facilitates resistance to cell death.

Conclusions:

  • SAMD is a critical factor in ovarian cancer progression and therapeutic resistance.
  • Measuring SAMD could provide a valuable biomarker for patient stratification.
  • Targeting SAMD presents a promising strategy for overcoming treatment resistance and restoring chemosensitivity.
Keywords:
Mitochondrial dynamicsMitochondrial dysfunctionOvarian cancerTargeted therapyTherapy resistance

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