ArticleCancers2022
Ferroptosis Induction and YAP Inhibition as New Therapeutic Targets in Gastrointestinal Stromal Tumors (GISTs).
Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- Ferroptosis in gastrointestinal stromal tumors.Journal of gastrointestinal oncology · 2026Article
- Non-Coding RNAs in Gastrointestinal Stromal Tumors: Regulatory Networks, Drug Resistance, and Clinical Implications.International journal of molecular sciences · 2026Review
- Different contributions of YAP1 and TAZ in the regulation of GIST tumorigenic properties.Cell communication and signaling : CCS · 2026Article
- The dual roles of ferroptosis in digestive tract tumors: mechanisms, microenvironment regulation, and therapeutic integration with emphasis on immune interactions.Frontiers in immunology · 2026Review
- β-elemene promotes ferroptosis to improve the sensitivity of imatinib in gastrointestinal stromal tumours by targeting N6AMT1.Clinical and translational medicine · 2025Article
- Toosendanin induces ferroptosis in gastrointestinal stromal tumor cells through the regulation of the NCOA4 ferritinophagy pathway: implications for tumor proliferation, migration, and invasion.Journal of gastrointestinal oncology · 2025Article
- Regulatory roles of non-coding RNAs in programmed cell death pathways and drug resistance in gastrointestinal stromal tumors.Clinical and experimental medicine · 2025Review
- Deubiquitinating enzymes: Key regulators of ferroptosis and pyroptosis and novel targets for cancer intervention.International journal of biological sciences · 2025Review
- Identification and validation of protein biomarkers for predicting gastrointestinal stromal tumor recurrence.Computational and structural biotechnology journal · 2024Article
- Advancing gastrointestinal stromal tumor management: The role of imagomics features in precision risk assessment.World journal of gastrointestinal surgery · 2024Article
- Verteporfin Exerts Anticancer Effects and Reverses Resistance to Paclitaxel via Inducing Ferroptosis in Esophageal Squamous Cell Cancer Cells.Molecular biotechnology · 2024Article
- Article
- KIT-SNAP-tag/cell membrane chromatography model coupled with liquid chromatography-mass spectrometry for anti-GIST compound screening from Evodia rutaecarpa.Analytical and bioanalytical chemistry · 2024Article
- TRIM21/USP15 balances ACSL4 stability and the imatinib resistance of gastrointestinal stromal tumors.British journal of cancer · 2024Article
- Article
- Ferroptosis: An Emerging Target for Bladder Cancer Therapy.Current issues in molecular biology · 2023Review
- Article
- Studying the Geroprotective Properties of YAP/TAZ Signaling Inhibitors onInternational journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
GISTs are sarcomas of the gastrointestinal tract often associated with gain-of-function mutations in KIT or PDGFRA receptor genes. While most GISTs initially respond to tyrosine kinase inhibitors, relapses due to acquired resistance frequently occur. The induction of ferroptosis, an iron-dependent form of non-apoptotic cell death, emerged as a novel therapeutic approach in cancers and remains poorly characterized in GISTs. We studied hallmarks of ferroptosis, i.e., lipid peroxidation, iron and glutathione content, and GPX4 protein expression in imatinib-sensitive (GIST882) and -resistant (GIST48) GIST cell lines. GIST cells were highly sensitive to the induction of ferroptosis by RSL3, which was reversed by liproxstatin and deferoxamine. Lipid peroxidation and ferroptosis were mediated by VP and CA3 in GIST cells through a significant decrease in antioxidant defenses. Moreover, VP, but surprisingly not CA3, inhibited a series of target genes downstream of YAP in GIST cells. The ferroptosis marker TFRC was also investigated by immunohistochemistry in GIST tissue arrays. TFRC expression was observed in all samples. High TFRC expression was positively correlated with high-risk GISTs, elevated mitotic count, and YAP nuclear localization, reflecting YAP activation. This study highlights ferroptosis as a novel cell death mechanism in GISTs, and a potential therapeutic target to overcome resistance to tyrosine kinase inhibitors.
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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 OpenQuestion graph.