ArticleBiological trace element research2026
Targeting the SOX11/GPX4/SLC7A11 Axis: A Novel Mechanism for Boric Acid-Induced Ferroptosis in Endometrial Cancer.
Article in Biological trace element research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Sex-determining region Y-related high-mobility group box 11 (SOX11) is recognized as a contributor to endometrial cancer (EC) progression, yet its specific involvement in ferroptosis regulation remains unclear. This research explores the potential of boric acid (BA) to influence both SOX11 expression and ferroptosis-related pathways within EC cells. Utilizing human EC-derived Ishikawa cells and non-malignant endometrial SHT290 cells, BA treatment regimens ranging from 100 µM to 25.6 mM were employed. Cellular viability and proliferative capacity were quantified using MTT and bromodeoxyuridine incorporation assays, respectively. Furthermore, quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and western blot analyses were conducted to evaluate the expression profiles of SOX11, glutathione peroxidase 4 (GPX4), and solute carrier family 7 member 11 (SLC7A11). Ferroptosis was evaluated through measurements of malondialdehyde (MDA), glutathione (GSH), Fe²⁺ content, and lipid peroxidation using the C11-BODIPY581/591 probe. BA reduced cell viability and proliferation in a time- and concentration-dependent manner, with IC₅₀ values of 2.6 mM and 15.5 mM in Ishikawa and SHT290 cells, respectively. In Ishikawa cells, BA induced detectable lipid peroxidation, cytomorphological changes, elevated MDA and Fe²⁺ levels, and depleted GSH content-hallmarks of ferroptosis. BA treatment decreased GPX4 and SLC7A11 expression while significantly downregulating SOX11 at both transcript and protein levels. These findings indicate that BA promotes ferroptosis and inhibits proliferation in EC cells, at least in part through suppression of SOX11 and downregulation of the GPX4/SLC7A11 axis. This study reveals a previously unreported regulatory mechanism and indicates that BA merits further investigation as a potential therapeutic agent targeting ferroptosis in EC.
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