ArticleCancer cell international2024
The clustering status of detached gastric cancer cells inhibits anoikis-induced ferroptosis to promote metastatic colonization.
Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 7 citations in OpenAlex.
- Ferroptosis and tumor microenvironment: orchestrating therapy resistance, immune evasion, and metastatic events.Medical oncology (Northwood, London, England) · 2026Review
- Bidirectional Feedback Between Metabolic Reprogramming and Epithelial-Mesenchymal Transition: From Mechanisms to Therapeutic Interventions.Molecules (Basel, Switzerland) · 2026Review
- Review
- YEATS2 promotes DNA repair and induces anoikis resistance by enhancing chromatin accessibility to drive prostate cancer metastasis.Oncogene · 2026Article
- PDHA1 enhances resistance to ferroptosis in anoikis-resistant prostate cancer by upregulating AIFM2.Cell death discovery · 2026Article
- Ferroptosis and metastasis: molecular checkpoints, microenvironmental dynamics, and therapeutic opportunities.Molecular cancer · 2026Review
- The Crosstalk Between Epithelial-Mesenchymal Transition and Anoikis Resistance: A New Perspective of Traditional Chinese Medicine to Prevent Tumor Metastasis.Drug design, development and therapy · 2026Review
- M2 macrophage-derived exosomes and miR-132-3p promote gastric cancer cell aggressiveness and attenuate ferroptosis-related changes.Frontiers in oncology · 2026Article
- Targeting ferroptosis inInternational journal of oncology · 2026Review
- Research progress on ferroptosis in drug resistance and therapy of gastric cancer.Journal of cancer research and clinical oncology · 2025Review
- Anoikis resistance in gastric cancer: a comprehensive review.Cell death & disease · 2025Review
- Identification of Anoikis-Related Genes in Gastric Cancer: Bioinformatics and Experimental Validation.Cancer medicine · 2025Article
- Construction and validation of a nomogram model for predicting peritoneal metastasis in gastric cancer based on ferroptosis-relate genes and clinicopathological features.Journal of gastrointestinal oncology · 2025Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
background and purposeFerroptosis is a form of regulated cell death characterized by iron-dependent lipid peroxidation. Its role in cancer metastasis remains unclear. In this study, we aimed to investigate the potential involvement of ferroptosis in gastric cancer (GC) metastasis.
methodsGC cells (AGS, MKN45, HGC27) were used to explore the role of ferroptosis in single and clustered cells with extracellular matrix (ECM) detachment in vitro. We overexpressed glutathione peroxidase 4 (GPX4) to inhibit ferroptosis and assessed the changes in cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). Then tumor tissues from 54 GC patients with and without lymphatic metastasis were collected for immunohistochemical staining to investigate the expression of ferroptosis and EMT markers. Finally, Kaplan-Meier survival curves were used to investigate the relationship between overall survival and expression of GPX4 in 178 GC patients.
resultsDetached single cells had lower viability than adherent cells, but cell clustering improved their survival under matrix-detached conditions. Detached single cells exhibited an induction of iron-dependent reactive oxygen species (ROS) accumulation, glutathione (GSH) depletion, lipid peroxidation, upregulation of ACSL4, TFRC and HO-1, increased iron levels, and changes in mitochondrial morphology. Opposite effects were observed in detached clustered cells, including the upregulation of the ferroptosis suppressors GPX4 and SLC7A11. Overexpression of GPX4 inhibited ferroptosis and promoted GC cell proliferation, migration, invasion, and EMT. Immunohistochemical analysis of tumor tissues from GC patients indicated that lymphatic metastasis was associated with higher potential for ferroptosis inhibition and EMT induction. Finally, Kaplan-Meier survival curves demonstrated a significant decrease in overall survival among GC patients with high GPX4 expression.
conclusionsOur study provides the first evidence that inhibition of ferroptosis is a crucial mechanism promoting GC metastasis. GPX4 may be a valuable prognostic factor for GC patients. These findings suggest that targeting ferroptosis inhibition may be a promising strategy for GC patients with metastatic potential. Trial registration The ethical approval code of this study in Institutional Review Board of Peking Union Medical College Hospital is No: K1447.
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