Zhou S, Cheng X, Zhang JM, Ji J, Ni ZZ, Wang W. Estrogen receptor 1 regulates ovarian cancer cell stemness and ferroptosis through modulation of the canonical RhoA/ROCK signaling pathway. World J Stem Cells 2026; 18(9): 121744 [DOI: 10.4252/wjsc.121744]
Corresponding Author of This Article
Wei Wang, Department of Pathology, Jiangsu Province Official Hospital, Geriatric Hospital of Nanjing Medical University, No. 65 Jiangsu Road, Nanjing 210009, Jiangsu Province, China. path_lucky@126.com
Research Domain of This Article
Oncology
Article-Type of This Article
research-article
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
Share the Article
Zhou S, Cheng X, Zhang JM, Ji J, Ni ZZ, Wang W. Estrogen receptor 1 regulates ovarian cancer cell stemness and ferroptosis through modulation of the canonical RhoA/ROCK signaling pathway. World J Stem Cells 2026; 18(9): 121744 [DOI: 10.4252/wjsc.121744]
World J Stem Cells. Sep 26, 2026; 18(9): 121744 Published online Sep 26, 2026. doi: 10.4252/wjsc.121744
Estrogen receptor 1 regulates ovarian cancer cell stemness and ferroptosis through modulation of the canonical RhoA/ROCK signaling pathway
Shun Zhou, Xue Cheng, Jing-Min Zhang, Jie Ji, Zhen-Zhen Ni, Wei Wang
Shun Zhou, Department of Interventional, Women’s Hospital of Nanjing Medical University, Nanjing Maternity and Child Health Care Hospital, Nanjing 210004, Jiangsu Province, China
Xue Cheng, Jing-Min Zhang, Jie Ji, Zhen-Zhen Ni, Department of Pathology, Women’s Hospital of Nanjing Medical University, Nanjing Maternity and Child Health Care Hospital, Nanjing 210004, Jiangsu Province, China
Wei Wang, Department of Pathology, Jiangsu Province Official Hospital, Geriatric Hospital of Nanjing Medical University, Nanjing 210009, Jiangsu Province, China
Author contributions: Zhou S and Wang W conceived and designed the study; Cheng X, Zhang JM, Ji J, and Ni ZZ performed data curation, methodology, and software analyses; Zhou S carried out the investigation, formal analysis, visualization, and wrote the original draft of the manuscript; Wang W handled project administration, resource acquisition, supervision, validation, and reviewed and edited the manuscript. All authors approved the final version.
AI contribution statement: No AI tools were used in the manuscript editing, figures, and data analysis.
Supported by the Talent Construction Fund Research Project of Jiangsu Province Geriatric Hospital, No. IR2024101.
Institutional review board statement: Clinical samples and experimental animals are not available in this paper.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: The raw data can be obtained on request from the corresponding author.
Corresponding author: Wei Wang, Department of Pathology, Jiangsu Province Official Hospital, Geriatric Hospital of Nanjing Medical University, No. 65 Jiangsu Road, Nanjing 210009, Jiangsu Province, China. path_lucky@126.com
Received: April 1, 2026 Revised: May 19, 2026 Accepted: August 28, 2026 Published online: September 26, 2026 Processing time: 177 Days and 3.8 Hours
Core Tip
Core Tip: This study investigated the effects of estrogen receptor 1 (ESR1) on ovarian cancer. Our findings revealed that ESR1, an overexpressed gene associated with cell stemness and ferroptosis in ovarian cancer, interacts with the Ras homolog (Rho) gene family member A/Rho-associated coiled-coil containing protein kinase signaling pathway. ESR1 knockdown in A2780 cells significantly decreased cell viability and proliferation, while increasing apoptosis. ESR1 silencing also reduced cell stemness (lowered aldehyde dehydrogenase, octamer-binding transcription factor 4, and Nanog) and promoted ferroptosis (increased Fe2+, ferritin heavy chain, and ferritin light chain, and decreased transferrin receptor 1). These inhibitory effects were reversed by treatment with CN03 (a Rho activator), demonstrating that ESR1 regulates ovarian cancer stemness and ferroptosis via the Ras homolog gene family member A/Rho-associated coiled-coil containing protein kinase signaling pathway.
