ArticleJournal of neuro-oncology2020
AKT/GSK-3β/β-catenin signaling pathway participates in erythropoietin-promoted glioma proliferation.
Article in Journal of neuro-oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Cyclooxygenase-2 as a potential therapeutic target in the treatment of chemoresistant glioblastomas.Medical oncology (Northwood, London, England) · 2025Review
- miR-542-3p attenuates corticosterone-induced hippocampal neuronal damage in depressive mice by modulating PTEN/AKT/GSK3β/β-catenin pathway.Biomolecules & biomedicine · 2025Article
- PNO1 enhances ovarian cancer cell growth, invasion, and stemness via activating the AKT/Wnt/β-catenin pathway.Scientific reports · 2025Article
- Phloroglucinol Enhances Anagen Signaling and Alleviates HJournal of microbiology and biotechnology · 2024Article
- Pyrogallol fromInternational journal of molecular sciences · 2023Article
- FAM84B promotes the proliferation of glioma cells through the cell cycle pathways.World journal of surgical oncology · 2022Article
- Article
- PCDH20 inhibits esophageal squamous cell carcinoma proliferation and migration by suppression of the mitogen-activated protein kinase 9/AKT/β-catenin pathway.Frontiers in oncology · 2022Article
- Neurodegeneration, memory loss, and dementia: the impact of biological clocks and circadian rhythm.Frontiers in bioscience (Landmark edition) · 2021Review
- The Role of PI3K/AKT and MAPK Signaling Pathways in Erythropoietin Signalization.International journal of molecular sciences · 2021Review
- Cognitive Impairment and Dementia: Gaining Insight through Circadian Clock Gene Pathways.Biomolecules · 2021Review
- GSK-3β Regulates the Expression of P21 to Promote the Progression of Chordoma.Cancer management and research · 2021Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAlthough erythropoietin (EPO) has been proven to significantly promote the proliferation of cancer cells, the mechanism for promoting glioma proliferation is poorly understood. Here, we examined the functional role of the AKT/GSK-3β/β-catenin signaling pathway in the EPO-mediated proliferation of glioma.
methodsThe distribution of EPO and Ki-67 among clinical samples with different WHO grades was plotted by Immunological Histological Chemistry analysis. U87 and U251 glioma cell lines were treated with short hairpin RNA targeting (shEPO), recombinant human erythropoietin (rhEPO) and/or AKT-specific inhibitor (MK-2206). The changes in phosphorylated AKT, nuclear β-catenin, cyclin D1 and p27kip1 expression were detected. Cell cycle distributions and glioma proliferation in vitro and in vivo were analyzed.
resultsThe expression level of EPO was significantly elevated with the increase of WHO grade and Ki67 in clinical glioma specimens. In vitro, knockdown of endogenous EPO in U87 and U251 cells effectively block the phosphorylation of AKT and GSK-3β and the expression of nuclear β-catenin. shEPO treatment also significantly decreased the expression of cyclin D1 and increased the expression of p27kip1. The cell cycle transition then slowed down and the proliferation of glioma cells or mouse xenograft tumors both decreased. Treatment of cells or tumors with extra rhEPO reversed the above biological effects mediated by shEPO. rhEPO-induced activation of the AKT/GSK-3β/β-catenin pathway and proliferation were abolished by MK-2206.
conclusionsOur study identified the AKT/GSK-3β/β-catenin axis as a critical mediator of EPO-induced glioma proliferation and further provided a clinically significant dimension to the biology of EPO.
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