Transcription factor FOXA1 suppresses ferroptosis of cervical cancer cells by upregulating SLC7A11 expression
- 1Department of Oncology, The Third Hospital of Mianyang (Sichuan Mental Health Center), No. 190, East Section of Jiannan Road, Mianyang City, 621000 Sichuan China
- 2Department of Radiology, The Third Hospital of Mianyang (Sichuan Mental Health Center), Mianyang City, 621000 Sichuan China
Abstract
Ferroptosis, a unique modality of cell death, possesses critical activity in tumorigenesis. This study defined the role of transcription factor (TF) forkhead box A1 (FOXA1) in modulating ferroptosis of cervical cancer (CC), a prevalent disease with high mortality rates in females. mRNA analysis was done by quantitative real-time PCR (qRT-PCR), and protein expression was analyzed by immunoblotting and immunohistochemistry (IHC). Colony formation and EdU proliferation assays were used to evaluate cell growth. Apoptosis was detected by flow cytometry. The contents of SOD, MDA, GSH, ROS and Fe2+ were measured by assay kits. Chromatin immunoprecipitation (ChIP)-qPCR and luciferase assays were applied to analyzed the binding of FOXA1 to the SLC7A11 promoter. FOXA1 was an overexpressed factor in CC, which was related to prognosis of human CC. FOXA1 downregulation impaired CC cell in vitro proliferation, promoted apoptosis, and induced ferroptosis. FOXA1 was validated to bind to the promoter of SLC7A11 and enhance SLC7A11 transcription. Furthermore, the FOXA1/SLC7A11 cascade affected proliferation, apoptosis and ferroptosis of CC cells. In addition, FOXA1 downregulation impeded the in vivo tumorigenesis of C33A CC cells. Our study has identified FOXA1 as a crucial repressor of CC cell ferroptosis depending on its activation of SLC7A11 transcription. Developing inhibitors of FOXA1 is a promising way of harnessing ferroptosis for CC treatment.
Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1186/s13008-026-00182-4.
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BibTeX
@article{gao2026transcription,
title = {{Transcription factor FOXA1 suppresses ferroptosis of cervical cancer cells by upregulating SLC7A11 expression}},
author = {Fei Gao and Yan Zeng and Li Jia and Jun He and Huarong He},
journal = {Cell Division},
year = {2026},
month = jun,
doi = {10.1186/s13008-026-00182-4},
url = {https://doi.org/10.1186/s13008-026-00182-4},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Transcription factor FOXA1 suppresses ferroptosis of cervical cancer cells by upregulating SLC7A11 expression
AU - Fei Gao
AU - Yan Zeng
AU - Li Jia
AU - Jun He
AU - Huarong He
PY - 2026
DA - 2026/06/25
JO - Cell Division
DO - 10.1186/s13008-026-00182-4
UR - https://doi.org/10.1186/s13008-026-00182-4
AB - Ferroptosis, a unique modality of cell death, possesses critical activity in tumorigenesis. This study defined the role of transcription factor (TF) forkhead box A1 (FOXA1) in modulating ferroptosis of cervical cancer (CC), a prevalent disease with high mortality rates in females. mRNA analysis was done by quantitative real-time PCR (qRT-PCR), and protein expression was analyzed by immunoblotting and immunohistochemistry (IHC). Colony formation and EdU proliferation assays were used to evaluate cell growth. Apoptosis was detected by flow cytometry. The contents of SOD, MDA, GSH, ROS and Fe2+ were measured by assay kits. Chromatin immunoprecipitation (ChIP)-qPCR and luciferase assays were applied to analyzed the binding of FOXA1 to the SLC7A11 promoter. FOXA1 was an overexpressed factor in CC, which was related to prognosis of human CC. FOXA1 downregulation impaired CC cell in vitro proliferation, promoted apoptosis, and induced ferroptosis. FOXA1 was validated to bind to the promoter of SLC7A11 and enhance SLC7A11 transcription. Furthermore, the FOXA1/SLC7A11 cascade affected proliferation, apoptosis and ferroptosis of CC cells. In addition, FOXA1 downregulation impeded the in vivo tumorigenesis of C33A CC cells. Our study has identified FOXA1 as a crucial repressor of CC cell ferroptosis depending on its activation of SLC7A11 transcription. Developing inhibitors of FOXA1 is a promising way of harnessing ferroptosis for CC treatment. Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1186/s13008-026-00182-4.
SN - 1747-1028
ER -