The dual role of autophagy in gynecologic malignancies: promoting and inhibiting
- 1Department of Traditional Chinese Medicine, Shandong Provincial Hospital Affiliated to Shandong First Medical University , ,
- 2School of Anesthesiology, Naval Medical University , ,
Abstract
Autophagy is a fundamental lysosome-dependent degradation pathway that maintains cellular homeostasis by recycling intracellular components. It plays a critical role in stress adaptation, energy metabolism, and genomic stability. Emerging evidence supports that autophagy exhibits a context-dependent dual role in the development and progression of gynecologic malignancies. In the early stages of tumorigenesis or under specific molecular conditions, autophagy exerts tumor-suppressive effects by preserving genomic integrity, attenuating chronic inflammation, and promoting autophagy-related cell death. However, as tumors progress or are exposed to therapeutic stress-such as radiotherapy, chemotherapy, or targeted therapy-autophagy is frequently reactivated as an adaptive survival mechanism. This process enhances tumor cell tolerance to metabolic stress, oxidative damage, and therapeutic interventions, thereby facilitating tumor progression and contributing to drug resistance. Accordingly, this review systematically summarizes the molecular regulatory mechanisms of autophagy in gynecologic malignancies and its role in treatment responses. Furthermore, it highlights the therapeutic potential of targeting autophagy to improve precision treatment strategies.
Related
- Spatial lipidomics in gynecologic malignancies: molecular identification, cellular attribution, and mechanistic validation.
- Proteasome Inhibitor MG132 Facilitates Antiviral Effects by Inhibiting TFEB Degradation and Activating Autophagy
- Knockdown of Smurf1 Promotes Autophagy-Dependent Ferroptosis in Acute Liver Failure by Inhibiting Ubiquitin-Mediated Ulk1 Degradation.
- Triple prophylaxis with fosaprepitant versus dual therapy for postoperative nausea and vomiting in high-risk gynecologic surgery
- Study on the Role of FHL2 in Chicken: Promoting Bone Growth and Inhibiting Fat Formation via Regulating BMSC Differentiation Balance.
BibTeX
@article{gai2026dual,
title = {{The dual role of autophagy in gynecologic malignancies: promoting and inhibiting}},
author = {Dongying Gai and Ning Jia and Fanghua Qi and Lizhou Song and Wenwen Shao and Lin Zhao and Pingping Cai},
journal = {Frontiers in cell and developmental biology},
year = {2026},
month = oct,
doi = {10.3389/fcell.2026.1968563},
url = {https://europepmc.org/article/PMC/PMC13717309},
note = {CC BY},
}
RIS
TY - JOUR
TI - The dual role of autophagy in gynecologic malignancies: promoting and inhibiting
AU - Dongying Gai
AU - Ning Jia
AU - Fanghua Qi
AU - Lizhou Song
AU - Wenwen Shao
AU - Lin Zhao
AU - Pingping Cai
PY - 2026
DA - 2026/10/15
JO - Frontiers in cell and developmental biology
DO - 10.3389/fcell.2026.1968563
UR - https://europepmc.org/article/PMC/PMC13717309
AB - Autophagy is a fundamental lysosome-dependent degradation pathway that maintains cellular homeostasis by recycling intracellular components. It plays a critical role in stress adaptation, energy metabolism, and genomic stability. Emerging evidence supports that autophagy exhibits a context-dependent dual role in the development and progression of gynecologic malignancies. In the early stages of tumorigenesis or under specific molecular conditions, autophagy exerts tumor-suppressive effects by preserving genomic integrity, attenuating chronic inflammation, and promoting autophagy-related cell death. However, as tumors progress or are exposed to therapeutic stress-such as radiotherapy, chemotherapy, or targeted therapy-autophagy is frequently reactivated as an adaptive survival mechanism. This process enhances tumor cell tolerance to metabolic stress, oxidative damage, and therapeutic interventions, thereby facilitating tumor progression and contributing to drug resistance. Accordingly, this review systematically summarizes the molecular regulatory mechanisms of autophagy in gynecologic malignancies and its role in treatment responses. Furthermore, it highlights the therapeutic potential of targeting autophagy to improve precision treatment strategies.
SN - 2296-634X
ER -