Adipocytes Protect Ovarian Cancer Cells from Ferroptosis
5 affiliations
- 1Department of Molecular Biology and Biophysics, University of Connecticut Health Center, Farmington, CT 06030, USA
- 2Statistical Consulting Services, Center for Open Research Resources and Support, University of Connecticut, Storrs, CT 06269, USA
- 3Department of Internal Medicine, Section on Molecular Medicine, Wake Forest University School of Medicine, Winston Salem, NC 27101, USA
- 4Department of Pathology and Laboratory Medicine, University of Connecticut Health Center, Farmington, CT 06030, USA
- 5Department of Immunology, University of Connecticut Health Center, Farmington, CT 06030, USA
Abstract
Ferroptosis is a regulated form of cell death driven by lipid oxidation. Induction of ferroptosis has emerged as a potential approach for cancer treatment. Work published by our group and others has suggested that ovarian cancer may be among the potential clinical targets of ferroptosis inducers. The microenvironment plays a key role in all ovarian cancers, including high-grade serous ovarian cancer (HGSOC). In particular, the adipocyte-rich omentum is an important metastatic niche for ovarian cancer peritoneal metastases. Given the pivotal role of adipocytes in the ovarian cancer microenvironment, in this work we sought to understand the contribution of adipocytes to ovarian cancer ferroptosis. We report that adipocytes and the adipocyte-conditioned medium (ACM) protect ovarian cancer cells from ferroptosis through a multifactorial process involving changes in membrane lipid composition and lipid sequestration. Inhibiting lipid transfer significantly enhanced the anti-tumor effect of erastin, a ferroptosis inducer, in immune-deficient mice bearing intraperitoneal ovarian tumors. Disabling this cytoprotective pathway may be key to the effective deployment of ferroptosis inducers in the treatment of ovarian cancer.
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BibTeX
@article{tesfay2026adipocytes,
title = {{Adipocytes Protect Ovarian Cancer Cells from Ferroptosis}},
author = {Lia Tesfay and Chaeyeon Yoo and Timothy E. Moore and Jingyun Lee and Kirtikar Shukla and Cristina M. Furdui and Poornima Hegde and Evan R. Jellison and Suzy V. Torti},
journal = {Biomolecules},
year = {2026},
month = sep,
doi = {10.3390/biom16101418},
url = {https://www.mdpi.com/2218-273X/16/10/1418},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Adipocytes Protect Ovarian Cancer Cells from Ferroptosis
AU - Lia Tesfay
AU - Chaeyeon Yoo
AU - Timothy E. Moore
AU - Jingyun Lee
AU - Kirtikar Shukla
AU - Cristina M. Furdui
AU - Poornima Hegde
AU - Evan R. Jellison
AU - Suzy V. Torti
PY - 2026
DA - 2026/09/30
JO - Biomolecules
DO - 10.3390/biom16101418
UR - https://www.mdpi.com/2218-273X/16/10/1418
AB - Ferroptosis is a regulated form of cell death driven by lipid oxidation. Induction of ferroptosis has emerged as a potential approach for cancer treatment. Work published by our group and others has suggested that ovarian cancer may be among the potential clinical targets of ferroptosis inducers. The microenvironment plays a key role in all ovarian cancers, including high-grade serous ovarian cancer (HGSOC). In particular, the adipocyte-rich omentum is an important metastatic niche for ovarian cancer peritoneal metastases. Given the pivotal role of adipocytes in the ovarian cancer microenvironment, in this work we sought to understand the contribution of adipocytes to ovarian cancer ferroptosis. We report that adipocytes and the adipocyte-conditioned medium (ACM) protect ovarian cancer cells from ferroptosis through a multifactorial process involving changes in membrane lipid composition and lipid sequestration. Inhibiting lipid transfer significantly enhanced the anti-tumor effect of erastin, a ferroptosis inducer, in immune-deficient mice bearing intraperitoneal ovarian tumors. Disabling this cytoprotective pathway may be key to the effective deployment of ferroptosis inducers in the treatment of ovarian cancer.
SN - 2218-273X
ER -