ArticleOncoTargets and therapy2019
CXCL8 Promotes Glioma Progression By Activating The JAK/STAT1/HIF-1α/Snail Signaling Axis.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- Identifying survival subtypes with autoencoder using multiple types of high-dimensional genomic data from studies of glioblastoma multiforme.Briefings in bioinformatics · 2025Article
- Mechanism of CXCL8 regulation of methionine metabolism to promote angiogenesis in gliomas.Discover oncology · 2024Article
- Immunotherapeutic Strategies for the Treatment of Glioblastoma: Current Challenges and Future Perspectives.Cancers · 2024Review
- Crosstalk between glioblastoma and tumor microenvironment drives proneural-mesenchymal transition through ligand-receptor interactions.Genes & diseases · 2024Review
- Hallmarks of the Tumour Microenvironment of Gliomas and Its Interaction with Emerging Immunotherapy Modalities.International journal of molecular sciences · 2023Review
- CHRM3 is a novel prognostic factor of poor prognosis and promotes glioblastoma progression via activation of oncogenic invasive growth factors.Oncology research · 2023Article
- Friends with Benefits: Chemokines, Glioblastoma-Associated Microglia/Macrophages, and Tumor Microenvironment.International journal of molecular sciences · 2022Review
- Tumour-associated CD204Neuropathology and applied neurobiology · 2022Article
- The versatile role of HuR in Glioblastoma and its potential as a therapeutic target for a multi-pronged attack.Advanced drug delivery reviews · 2022Review
- Construction of Molecular Subtypes and Related Prognostic and Immune Response Models Based on M2 Macrophages in Glioblastoma.International journal of general medicine · 2022Article
- The mechanism of colon tissue damage mediated by HIF-1α/NF-κB/STAT1 in high-altitude environment.Frontiers in physiology · 2022Article
- Evaluation of Comprehensive Gene Expression and NK Cell-Mediated Killing in Glioblastoma Cell Line-Derived Spheroids.Cancers · 2021Article
- Review
- Review
- Prediction and analysis of hub genes between glioblastoma and low-grade glioma using bioinformatics analysis.Medicine · 2021Article
- The Role of Selected Chemokines and Their Receptors in the Development of Gliomas.International journal of molecular sciences · 2020Review
Corrections and comments
- Retraction · 2023-03-28Concerns/Issues about Data · Duplication of/in Image · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundUpregulation of CXCL8 (C-X-C motif ligand 8) in tumor cells has been reported in several types of cancer, and it correlates with a poor prognosis. However, the role of CXCL8 in glioma progression remains unknown. MATERIALS AND
methodsIn this study, we examined CXCL8 expression levels in human glioma cell lines and in sixteen human gliomas with different grades. The molecular role of CXCL8 in glioma cells was investigated using quantitative polymerase chain reaction (qRT-PCR) assays, Western blotting, CCK-8 assays, EdU assays, colony formation assays, Transwell migration and invasion assays.
resultsWe found that high expression levels of CXCL8 were positively associated with progression and poor prognosis in human glioma. Mechanistically, CXCL8 promoted the epithelial-mesenchymal transition (EMT) in glioma cells by activating the JAK/STAT1/HIF-1α/Snail signaling pathway.
conclusionTaken together, our data provide a plausible mechanism for CXCL8-modulated glioma progression, which suggests that CXCL8 may represent a potential therapeutic target in the prevention and treatment of gliomas.
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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.