ArticleCurrent cancer drug targets2025
Silencing HEATR1 Rescues Cisplatin Resistance of Non-small Cell Lung Cancer by Inducing 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 9 papers.
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The trial behind it
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Who cites it
9 citing papers in PubMed.
- TWF1 inhibition overcomes cisplatin resistance in NSCLC by inducing ferroptosis via p53-dependent SLC7A11 repression and autophagy-mediated glutathione metabolism reprogramming.Cancer gene therapy · 2026Article
- HEATR1 deficiency enhanced gastric cancer cell PANoptosis to boost anti-tumor immunity.Molecular medicine (Cambridge, Mass.) · 2026Article
- Cardiovascular Toxicity in Cancer Therapy: Potential Mechanisms of Ferroptosis and Treatment Strategies.Cells · 2026Review
- The cross-talk and interplay between ferroptosis and cuproptosis in tumor and therapeutics.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Natural products reshape osteosarcoma cell fate: promoting cell death.Frontiers in pharmacology · 2026Review
- A novel ferroptosis-related microRNAs signature for predicting prognosis in endometrial cancer: An observational study.Medicine · 2025Observational
- The Molecular Interplay Between p53-Mediated Ferroptosis and Non-Coding RNAs in Cancer.International journal of molecular sciences · 2025Review
- Review
- Targeting MGST1 Makes Non-Small Cell Lung Cancer Cells Sensitive to Radiotherapy by Epigenetically Enhancing ALOX15-Mediated Ferroptosis.Current cancer drug targets · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundCisplatin (DDP) is a commonly used chemotherapy agent. However, its resistance to the drug is a major challenge in its clinical application. Earlier research has suggested a connection between HEATR1 and chemoresistance in cancer. However, additional investigation is needed to better understand its involvement in resistance to DDP. In this study, we aimed to determine the regulatory effect of HEATR1 on the resistance of cisplatin in NSCLC.
methodsWe collected specimens of both DDP-resistant and non-resistant NSCLC to examine the expression of HEATR1. Additionally, we established cisplatin-resistant cells of NSCLC using the A549 cell line. Cell ability was examined by CCK-8 assay. Cell apoptosis and lipid ROS were examined by flow cytometry. The expressions of HEATR1, p53, SAT1, and ALOX15 were determined by qRT-PCR and Western blot. The tumor xenograft experiment was conducted to assess the impact of silencing HEATR1 on cisplatin resistance
resultsThe expression levels of HEATR1 were found to be significantly elevated in DDP-resistant tissues and cells of NSCLC as compared to non-resistant counterparts. Conversely, the expression levels of p53, SAT1, and ALOX15 were observed to be reduced in DDP-resistant cells. Through the inhibition of HEATR1, the proliferation of DDP-resistant cells was significantly suppressed, while the generation of lipid ROS was enhanced. This effect was achieved by activating ferroptosis and the p53/SAT1/ALOX15 pathway, as demonstrated both
conclusionFinally, the findings revealed that HEATR1 silencing reduced DDP resistance in NSCLC by inducing ferroptosis via the p53/SAT1/ALOX15 axis. HEATR1 might become a potential target for overcoming DDP resistance in NSCLC treatment.
Indexed as
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.