ArticleEsophagus : official journal of the Japan Esophageal Society2023
Simultaneous regulation of ferroptosis suppressor protein 1 and glutathione peroxidase 4 as a new therapeutic strategy of ferroptosis for esophageal squamous cell carcinoma.
Article in Esophagus : official journal of the Japan Esophageal Society, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Ferroptosis is a protective factor for the prognosis of cancer patients: a systematic review and meta-analysis.BMC cancer · 2024Pooled it
- Metabolic control of ferroptosis in cancer: lipid dependencies as therapeutic vulnerabilities.Frontiers in oncology · 2026Review
- The Role of Mitochondrial DNA in Modulating Chemoresistance in Esophageal Cancer: Mechanistic Insights and Therapeutic Potential.Biomolecules · 2025Review
- Review
- GPX4 and FSP1 Expression in Lung Adenocarcinoma: Prognostic Implications and Ferroptosis-Based Therapeutic Strategies.Cancers · 2024Article
- Ferroptosis: Biology and Role in Gastrointestinal Disease.Gastroenterology · 2024Review
- Prognostic significance and therapeutic potential of guanosine triphosphate cyclohydrolase 1 in esophageal squamous cell carcinoma: clinical implications of ferroptosis and lipid peroxidation regulation.Frontiers in oncology · 2024Article
- GPX4 overexpression does not alter atherosclerotic plaque development in ApoE knock-out mice.Vascular biology (Bristol, England) · 2024Article
- [Dual inhibition of PSME2 and STAT3 induces ferroptosis in esophageal squamous cell carcinoma cells by regulating the SLC7A11/GPX4 axis].Nan fang yi ke da xue xue bao = Journal of Southern Medical UniversityArticle
Corrections and comments
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11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFerroptosis suppressor protein 1 and glutathione peroxidase 4 have been identified as key molecules in two independent pathways associated with ferroptosis inhibition. This study investigated the prognostic significance and clinical associations of FSP1 and GPX4 expression in esophageal squamous cell carcinoma (ESCC) and assessed the therapeutic potential of regulating these molecules in ESCC cells.
methodsImmunohistochemical analysis was performed on surgical specimens of 97 patients with ESCC for FSP1 and GPX4 expression. To identify the change in ESCC cell viability, FSP1 and GPX4 inhibitors were administered to three cell lines. In addition, ferroptosis as the cause of reduced cell viability by FSP1 and GPX4 inhibition was confirmed.
resultsPrognosis was significantly worse for patients in the group positive for both FSP1 and GPX4 compared with the other groups (p < 0.001). In multivariate analysis, positivity for both FSP1 and GPX4 was an independent poor prognostic factor (p = 0.002). The combination of FSP1 and GPX4 inhibitors induced cell death more potently than each inhibitor did alone. Furthermore, the ferroptosis inhibitor markedly canceled this cell death.
conclusionsOverexpression of FSP1 and GPX4 is a poor prognostic factor for patients with ESCC. Simultaneous suppression of both FSP1 and GPX4 caused potent cell death, which was markedly abrogated by ferroptosis inhibitors. These findings indicate that simultaneous regulation of FSP1 and GPX4 may be a new therapeutic target in ESCC.
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