ArticleMolecular biology reports2025
GSK-3 inhibitor induces apoptosis and cell cycle arrest in CD133
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Metabolic reprogramming and plasticity of cancer stem cells.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
backgroundTreatment of advanced prostate cancer (PCa) is a major challenge due to the persistence of drug-resistant cancer stem cells (CSCs), which are mainly responsible for metastasis and recurrence. Therefore, the key to achieve an effective treatment approach in PCa is through the development of strategies targeting CSCs. GSK-3, also known as a moonlight kinase, is associated with multiple signaling pathways involved in embryonic development and cancer, including Wnt/β-catenin, Sonic hedgehog, and Notch. Strong evidence suggests that pharmacological inhibition of GSK-3 can eliminate the prostate cancer stem/progenitor-like population. The present study aims to evaluate the effects of GSK-3 inhibitor IX on CD133 METHODS AND
resultsFollowing treatment with various concentrations of GSK-3 inhibitor IX, we assessed cell viability, apoptosis, cell cycle, and multicellular tumor spheroids formation capacity. Furthermore, expression levels of components in the Notch signaling pathway due to GSK-3 inhibition were examined by immunofluorescence staining. The results revealed that GSK-3 inhibitor IX exhibited strong anti-proliferative effects by inducing apoptotic cell death, causing G0/G1 phase arrest of CD133
conclusionTogether, our data demonstrated that GSK-3 inhibitor IX effectively eliminated CD133
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