ArticleCurrent cancer drug targets2025
Targeting MGST1 Makes Non-Small Cell Lung Cancer Cells Sensitive to Radiotherapy by Epigenetically Enhancing ALOX15-Mediated Ferroptosis.
Article in Current cancer drug targets, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- GSH-Related Enzymes GPx4, Chac1, and GSTs and Redox Regulation of Ferroptosis in Cancer.International journal of molecular sciences · 2026Review
- Inducing Ferroptosis: Sensitization Strategy for Radiotherapy and Its Application.Antioxidants (Basel, Switzerland) · 2026Review
- Targeting ferroptosis in lung cancer: pharmacological regulation, nanomedicine-based delivery, and AI-enabled translational strategies.American journal of cancer research · 2026Review
- From mitochondrial dysregulation to ferroptosis: Exploring new strategies and challenges in radioimmunotherapy (Review).International journal of oncology · 2025Review
- Targeting ferroptosis: a promising approach for treating lung carcinoma.Cell death discovery · 2025Review
- Macranthoside B Suppresses the Growth of Adenocarcinoma of Esophagogastric Junction by Regulating Iron Homeostasis and Ferroptosis through NRF2 Inhibition.Current cancer drug targets · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
backgroundFerroptosis is closely related to radiotherapy resistance in multiple cancers. Herein, the role of microsomal glutathione S-transferase 1 (MGST1) in regulating ferroptosis and radiotherapy resistance in non-small cell lung cancer (NSCLC) was investigated.
methodsRadiation-resistant NSCLC cells (NCI-1299-IR and HCC827-IR cells) were established. After exposure to X-ray, cell proliferation and survival were assessed by colony formation assay and CCK-8 assay, and lipid ROS level was examined by the fluorophore BODIPY™ 581/591 C11. MDA, GSH, and Fe
resultsOur results showed that RSL3 treatment greatly enhanced the radiotherapy sensitivity of NCI-1299-IR and HCC827-IR cells. It was subsequently revealed that MGST1 was highly expressed in NCI-1299-IR and HCC827-IR cells than its parent cells, and silencing of MGST1 reduced radioresistance of NCI-1299-IR and HCC827-IR cells by facilitating ferroptosis. Mechanistically, MGST1 knockdown greatly reduced HO-1 and DNMT1/3A protein levels, leading to reduced DNA methylation on the ALOX15 promoter region, thereby epigenetically upregulating ALOX15 expression. As expected, the promoting effects of MGST1 silencing on radiosensitivity and ferroptosis in radiation-resistant NSCLC cells were strikingly eliminated by ALOX15 knockdown.
conclusionMGST1 knockdown epigenetically enhanced radiotherapy sensitivity of NCSLC cells by promoting ALOX15-mediated ferroptosis through regulating the HO-1/DNMT1 pathway.
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