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Updated: May 18, 2026

An Ex Vivo Model of Ovarian Cancer Peritoneal Metastasis Using Human Omentum
Published on: January 26, 2024
Involvement of autophagy in ovarian cancer: a working hypothesis
Claudia Peracchio1, Oscar Alabiso, Guido Valente
1Laboratory of Molecular Pathology and Nanobioimaging, Department of Health Sciences, Novara, Italy. isidoro@med.unipmn.it.
Abstract:
Autophagy is a lysosomal-driven catabolic process that contributes to preserve cell and tissue homeostases through the regular elimination of damaged, aged and redundant self-constituents. In normal cells, autophagy protects from DNA mutation and carcinogenesis by preventive elimination of pro-oxidative mitochondria and protein aggregates. Mutations in oncogenes and oncosuppressor genes dysregulate autophagy. Up-regulated autophagy may confer chemo- and radio-resistance to cancer cells, and also a pro-survival advantage in cancer cells experiencing oxygen and nutrient shortage. This fact is the rationale for using autophagy inhibitors along with anti-neoplastic therapies. Yet, aberrant hyper-induction of autophagy can lead to cell death, and this phenomenon could also be exploited for cancer therapy. The actual level of autophagy in the cancer cell is greatly affected by vascularization, inflammation, and stromal cell infiltration. In addition, small non-coding microRNAs have recently emerged as important epigenetic modulators of autophagy. The present review focuses on the potential involvement of macroautophagy, and on its genetic and epigenetic regulation, in ovarian cancer pathogenesis and progression.
Insights
Autophagy, a cellular recycling process, plays a dual role in cancer. Inhibiting autophagy can enhance cancer treatment, while its overactivation may induce cancer cell death.
Area of Science:
- Cell Biology
- Molecular Biology
- Oncology
Background:
- Autophagy is a fundamental cellular process essential for maintaining homeostasis by clearing damaged components.
- In normal cells, autophagy prevents DNA mutations and cancer by eliminating harmful mitochondria and protein aggregates.
- Dysregulation of autophagy, often due to genetic mutations, is implicated in cancer development and progression.
Purpose of the Study:
- To review the role of macroautophagy in ovarian cancer pathogenesis and progression.
- To explore the genetic and epigenetic regulation of autophagy in the context of ovarian cancer.
- To discuss the therapeutic implications of modulating autophagy in ovarian cancer treatment.
Main Methods:
- Literature review focusing on macroautophagy.
- Analysis of genetic and epigenetic regulation of autophagy.
- Examination of autophagy's role in cancer cell survival and death.
Main Results:
- Autophagy can promote cancer cell survival under stress (hypoxia, nutrient deprivation) and confer resistance to chemotherapy and radiotherapy.
- Aberrant hyper-induction of autophagy can lead to cancer cell death, presenting a potential therapeutic strategy.
- Factors like vascularization, inflammation, stromal infiltration, and microRNAs significantly influence autophagy levels in cancer cells.
Conclusions:
- Autophagy's complex role in ovarian cancer necessitates careful consideration for therapeutic strategies.
- Targeting autophagy, either through inhibition or induction, holds promise for ovarian cancer treatment.
- Understanding the genetic and epigenetic control of autophagy is crucial for developing effective cancer therapies.
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