# Subcellular Stress Markers in Epithelial Ovarian Cancer

## TL;DR

This review explores how subcellular stress markers contribute to epithelial ovarian cancer and their potential as biomarkers and treatments.

## Contribution

The paper systematically summarizes the role of mitochondrial and ER stress markers in epithelial ovarian cancer pathogenesis and therapeutic targeting.

## Key findings

- Mitochondrial and ER stress contribute significantly to epithelial ovarian cancer progression.
- Proteins like MARCH5, AKAPs, and UPRmt proteins are highlighted as potential therapeutic targets.
- Many identified stress markers are in preclinical stages but show promise for future treatments.

## Abstract

Epithelial ovarian cancer is one of the most lethal gynecological malignancies worldwide. Its development strongly depends on several genetic and environmental factors, with metabolic components and cellular redox homeostasis alterations playing a significant a role in its development and disease progression. In this review, we summarize the contribution of mitochondrial and endoplasmic reticulum (ER) stress in the pathogenesis of epithelial ovarian cancer along with their role as potential biomarkers and therapeutic targets, including proteins of glucose metabolism, mitochondrial fission and fusion, mitophagy, membrane-associated ring-CH-type finger 5 (MARCH5), A-kinase anchoring proteins (AKAPs), proteins regulating mitochondrial Ca2+ homeostasis, mitochondrial unfolded protein response (UPRmt) proteins, activating transcription factors (ATFs), CCAAT enhancer binding protein (C/EBP) homologous protein (CHOP), ‘mitokines’, GRP75, and GRP78. Although many of these potential targets are in preclinical phase, they have a high potential to become valuable alternative or additive treatments for epithelial ovarian cancers.