ArticleCell & bioscience2025
Cholesterol confers resistance to Apatinib-mediated ferroptosis in gastric cancer.
Article in Cell & bioscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
7 citing papers in PubMed.
- Site-specific cholesterol depletion therapy for gastric cancer.Journal of lipid research · 2026Article
- Redox-regulated cell death in gastric cancer: Molecular insights and therapeutic opportunities.Journal of physiology and biochemistry · 2026Review
- Repurposing azole antifungals as rapid bactericidal, membrane-disruptive therapeutics againstMicrobiology spectrum · 2026Article
- Bidirectional crosstalk between ER stress and lipid metabolism: From proteostasis to tumor adaptation.Cell death discovery · 2025Review
- Cholesterol metabolism and cancer: Molecular mechanisms, immune regulation and an epidemiological perspective (Review).International journal of molecular medicine · 2025Review
- Recent advances in understanding the relationship between lipid metabolism and immune escape in the tumor microenvironment of gastric cancer.Medical review (2021) · 2025Review
- HMGCR: a malignancy hub - frontiers in cancer diagnosis and therapy.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
backgroundGastric cancer is the fifth leading cause of cancer-related deaths worldwide. Apatinib is a third-line treatment for gastric cancer. However, the development of resistance significantly limits its efficacy, and effective and safe strategies to overcome Apatinib resistance remain elusive.
resultsWe found that Apatinib-resistant gastric cancer cells (MGC803/AR and AGS/AR) exhibited increased cholesterol synthesis and elevated intracellular cholesterol levels, which contributed to Apatinib resistance. Further investigation identified 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) as one of the most upregulated genes in the cholesterol synthesis pathway. Inhibition of HMGCR not only suppressed the proliferation, migration, and invasion of resistant cells but also reduced their resistance to Apatinib. Moreover, Simvastatin, an HMGCR inhibitor, effectively resensitized resistant cells to Apatinib-induced ferroptosis, thereby enhancing the therapeutic efficacy of Apatinib both in vitro and in vivo.
conclusionsThese findings suggest that Simvastatin may serve as a novel and safe strategy to overcome Apatinib resistance in gastric cancer.
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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.