ArticleOncogenesis2012
Selective growth inhibition by glycogen synthase kinase-3 inhibitors in tumorigenic HeLa hybrid cells is mediated through NF-κB-dependent GLUT3 expression.
Article in Oncogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- AZD1080, a specific inhibitor of GSK‑3β, inhibits stemness and malignancies in osteosarcoma cancer stem‑like cells.Molecular medicine reports · 2025Article
- Progress of research on glucose transporter proteins in hepatocellular carcinoma.World journal of hepatology · 2025Review
- Bergaptol Ameliorates Insulin Sensitivity in Gestational Diabetes Mellitus by Inhibiting the Inflammatory Pathway in Streptozotocin-Induced Diabetic Rats.Physiological research · 2025Article
- Envisioning Glucose Transporters (GLUTs and SGLTs) as Novel Intervention against Cancer: Drug Discovery Perspective and Targeting Approach.Current drug targets · 2025Review
- The potential regulatory role of the lncRNA-miRNA-mRNA axis in teleost fish.Frontiers in immunology · 2023Review
- Identification of lactylation related model to predict prognostic, tumor infiltrating immunocytes and response of immunotherapy in gastric cancer.Frontiers in immunology · 2023Article
- Expression and Prognostic Value of Glucose Transporter 3 in Diffuse Large B Cell Lymphoma.OncoTargets and therapy · 2022Article
- Glucose Transporters as a Target for Anticancer Therapy.Cancers · 2021Review
- Article
- CD205Cancer science · 2021Article
- Functional miR-142a-3p Induces Apoptosis and Macrophage Polarization by TargetingFrontiers in immunology · 2021Article
- GLUT3 upregulation promotes metabolic reprogramming associated with antiangiogenic therapy resistance.JCI insight · 2017Article
- An Oncogenic Virus Promotes Cell Survival and Cellular Transformation by Suppressing Glycolysis.PLoS pathogens · 2016Article
- Metabolic targets for cancer therapy.Nature reviews. Drug discovery · 2013Review
- Concerted suppression of STAT3 and GSK3β is involved in growth inhibition of non-small cell lung cancer by Xanthatin.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Carcinogenesis and cancer progression, driven by mutations in oncogenes and tumor-suppressor genes, result in biological differences between normal and cancer cells in various cellular processes. Specific genes and signaling molecules involved in such cellular processes may be potential therapeutic targets of agents that specifically interact with the key factors in cancer cells. Increased glucose uptake is fundamental to many solid tumors and well associated with increases in glycolysis and the overexpression of glucose transporters (GLUTs) such as GLUT1 and GLUT3 at the plasma membrane. Here, we used cell-based screening to identify glycogen synthase kinase-3β (GSK-3β) inhibitors that selectively target GLUT3-expressing tumorigenic HeLa cell hybrids as compared with non-tumorigenic hybrids that express GLUT1 alone. The GSK-3 inhibitors as well as GSK-3β RNAi suppressed GLUT3 expression at the level of transcription, leading to apoptosis. This suppression was associated with NF-κB in a p53-independent manner. Furthermore, GSK-3 inhibitors exhibited a synergistic effect with anticancer agents such as adriamycin and camptothecin in GULT3-overexpressing colon cancer cells, but little effect in non-producing A431 cells. These results suggest a potential use of GSK-3 inhibitors to selectively kill cancer cells that overexpress GLUT3.
Identifiers
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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 OpenQuestion graph.