ArticleOxidative medicine and cellular longevity2022
Apatinib Induces Ferroptosis of Glioma Cells through Modulation of the VEGFR2/Nrf2 Pathway.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Systematic Review of Molecular Targeted Therapies for Adult-Type Diffuse Glioma: An Analysis of Clinical and Laboratory Studies.International journal of molecular sciences · 2023Pooled it
- Apatinib and silver nanoparticles synergize against gastric cancer through the PI3K/Akt signaling pathway-mediated ferroptosis.Journal of pharmaceutical analysis · 2026Article
- Comprehensive exploration of the role of multimodal programmed cell death- associated lncRNAs in the prognosis and immunity of glioma.Frontiers in immunology · 2026Article
- Ferroptosis as a therapeutic target in glioblastoma: Mechanisms and emerging strategies.Molecular therapy. Nucleic acids · 2025Review
- Programmed cell death disrupts inflammatory tumor microenvironment (TME) and promotes glioblastoma evolution.Cell communication and signaling : CCS · 2024Review
- YY1: a key regulator inhibits gastric cancer ferroptosis and mediating apatinib-resistance.Cancer cell international · 2024Article
- S670, an amide derivative of 3-O-acetyl-11-keto-β-boswellic acid, induces ferroptosis in human glioblastoma cells by generating ROS and inhibiting STX17-mediated fusion of autophagosome and lysosome.Acta pharmacologica Sinica · 2024Article
- Treatment advances in high-grade gliomas.Frontiers in oncology · 2024Review
- Nrf2 in human cancers: biological significance and therapeutic potential.American journal of cancer research · 2024Review
- A pH-Responsive Drug-Delivery System Based on Apatinib-Loaded Metal-Organic Frameworks for Ferroptosis-Targeted Synergistic Anti-Tumor Therapy.International journal of nanomedicine · 2024Article
- Molecular Targeted Therapies in Glioblastoma Multiforme: A Systematic Overview of Global Trends and Findings.Brain sciences · 2023Review
- Knockdown of HNRNPM inhibits the progression of glioma through inducing ferroptosis.Cell cycle (Georgetown, Tex.) · 2023Article
- Targeting vascular normalization: a promising strategy to improve immune-vascular crosstalk in cancer immunotherapy.Frontiers in immunology · 2023Review
- Opportunities and challenges related to ferroptosis in glioma and neuroblastoma.Frontiers in oncology · 2023Review
- Article
- Nrf2 signaling pathway: current status and potential therapeutic targetable role in human cancers.Frontiers in oncology · 2023Review
- Targeting cell death pathways for cancer therapy: recent developments in necroptosis, pyroptosis, ferroptosis, and cuproptosis research.Journal of hematology & oncology · 2022Review
- Multi-target tyrosine kinase inhibitor nanoparticle delivery systems for cancer therapy.Materials today. Bio · 2022Review
- Identification and Validation of a Novel Ferroptotic Prognostic Genes-Based Signature of Clear Cell Renal Cell Carcinoma.Cancers · 2022Article
- Ferroptosis Modulation: Potential Therapeutic Target for Glioblastoma Treatment.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Glioma is a common tumor that originated from the brain, and molecular targeted therapy is one of the important treatment modalities of glioma. Apatinib is a small-molecule tyrosine kinase inhibitor, which is widely used for the treatment of glioma. However, the underlying molecular mechanism has remained elusive. Recently, emerging evidence has proved the remarkable anticancer effects of ferroptosis. In this study, a new ferroptosis-related mechanism of apatinib inhibiting proliferation of glioma cells was investigated, which facilitated further study on inhibitory effects of apatinib on cancer cells. Methods: Human glioma U251 and U87 cell lines and normal astrocytes were treated with apatinib. Ferroptosis, cell cycle, apoptosis, and proliferation were determined. A nude mouse xenograft model was constructed, and tumor growth rate was detected. Tumor tissues were collected to estimate ferroptosis levels and to identify the relevant pathways after treatment with apatinib. Results: Treatment with apatinib could induce loss of cell viability of glioma cells, but not of normal astrocytes, through eliciting ferroptosis in vitro and in vivo. It was also revealed that apatinib triggered ferroptosis of glioma cells via inhibiting the activation of nuclear factor erythroid 2-related factor 2/vascular endothelial growth factor receptor 2 (Nrf2/VEFGR2) pathway. The overexpression of Nrf2 rescued the therapeutic effects of apatinib. Conclusion: Our study proved that treatment with apatinib could restrain proliferation of glioma cells through induction of ferroptosis via inhibiting the activation of VEGFR2/Nrf2/Keap1 pathway. Overexpression of Nrf2 could counteract the induction of ferroptosis by apatinib.
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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.