ArticleInternational journal of molecular sciences2020
CAIX Regulates GBM Motility and TAM Adhesion and Polarization through EGFR/STAT3 under Hypoxic Conditions.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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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, 24 citations in OpenAlex.
- Von Hippel-Lindau/Hypoxia Inducible Factor Axis in Glioblastoma.International journal of molecular sciences · 2025Review
- Co-culture models for investigating cellular crosstalk in the glioma microenvironment.Cancer pathogenesis and therapy · 2024Review
- Metabolic Roles of HIF1, c-Myc, and p53 in Glioma Cells.Metabolites · 2024Review
- Crosstalk between glioblastoma and tumor microenvironment drives proneural-mesenchymal transition through ligand-receptor interactions.Genes & diseases · 2024Review
- Gene Targets of CAR-T Cell Therapy for Glioblastoma.Cancers · 2023Review
- Exosome-based nanoimmunotherapy targeting TAMs, a promising strategy for glioma.Cell death & disease · 2023Review
- CAR T cells: engineered immune cells to treat brain cancers and beyond.Molecular cancer · 2023Review
- Carbonic Anhydrase IX Expression and Treatment Response Measured in Rectal Adenocarcinoma Following Neoadjuvant Chemo-Radiotherapy.International journal of molecular sciences · 2023Article
- ROS regulation in gliomas: implications for treatment strategies.Frontiers in immunology · 2023Review
- Natural killer cell awakening: unleash cancer-immunity cycle against glioblastoma.Cell death & disease · 2022Review
- Galectin-1 activates carbonic anhydrase IX and modulates glioma metabolism.Cell death & disease · 2022Article
- Article
- Hypoxia-Driven M2-Polarized Macrophages Facilitate Cancer Aggressiveness and Temozolomide Resistance in Glioblastoma.Oxidative medicine and cellular longevity · 2022Article
- Origin, activation, and targeted therapy of glioma-associated macrophages.Frontiers in immunology · 2022Review
- Signal Pathways Involved in the Interaction Between Tumor-Associated Macrophages/TAMs and Glioblastoma Cells.Frontiers in oncology · 2022Review
- The Acidic Brain-Glycolytic Switch in the Microenvironment of Malignant Glioma.International journal of molecular sciences · 2021Review
- Context-Dependent Glioblastoma-Macrophage/Microglia Symbiosis and Associated Mechanisms.Trends in immunology · 2021Review
- Carbonic Anhydrases as Potential Targets Against Neurovascular Unit Dysfunction in Alzheimer's Disease and Stroke.Frontiers in aging neuroscience · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Carbonic anhydrases (CAs) are acid-base regulatory proteins that modulate a variety of physiological functions. Recent findings have shown that CAIX is particularly upregulated in glioblastoma multiforme (GBM) and is associated with a poor patient outcome and survival rate. An analysis of the GSE4290 dataset of patients with gliomas showed that CAIX was highly expressed in GBM and was negatively associated with prognosis. The expression of CAIX under hypoxic conditions in GBM significantly increased in protein, mRNA, and transcriptional activity. Importantly, CAIX upregulation also regulated GBM motility, monocyte adhesion to GBM, and the polarization of tumor-associated monocytes/macrophages (TAM). Furthermore, the overexpression of CAIX was observed in intracranial GBM cells. Additionally, epidermal growth factor receptor/signal transducer and activator of transcription 3 regulated CAIX expression under hypoxic conditions by affecting the stability of hypoxia-inducible factor 1α. In contrast, the knockdown of CAIX dramatically abrogated the change in GBM motility and monocyte adhesion to GBM under hypoxic conditions. Our results provide a comprehensive understanding of the mechanisms of CAIX in the GBM microenvironment. Hence, novel therapeutic targets of GBM progression are possibly developed.
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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.