ArticleBlood2007
Inhibition of glycogen synthase kinase-3 activity leads to epigenetic silencing of nuclear factor kappaB target genes and induction of apoptosis in chronic lymphocytic leukemia B cells.
Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 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.
The trial behind it
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
103 citing papers in PubMed, 189 citations in OpenAlex.
- Elraglusib, a Glycogen Synthase Kinase 3β Inhibitor, plus Chemotherapy with or without Immunotherapy in Patients with Recurrent, Metastatic Salivary Gland Carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Trial
- Overcoming resistance to antibody-drug conjugates: mechanisms and emerging strategies.The oncologist · 2026Review
- Drug resistance in chronic myeloid leukemia: the involvement of Galectin-1 and Galectin-3.Molecular biology reports · 2026Review
- Inhibition of glycolysis and stimulation of mitochondrial biogenesis lead to increased ROS levels and cell death in HNF-1ß positive clear cell carcinoma.Cell death & disease · 2025Article
- ThemBio · 2025Article
- Signaling networks and MiRNA crosstalk in ovarian cancer chemoresistance.Journal of ovarian research · 2025Review
- Glycogen synthase kinase 3β: a key player in progressive chronic kidney disease.Clinical science (London, England : 1979) · 2025Review
- miR-32-5p suppresses the progression of hepatocellular carcinoma by regulating the GSK3β/NF-κB signaling.Acta biochimica et biophysica Sinica · 2025Article
- Article
- NF-κB Transcription Factors: Their Distribution, Family Expansion, Structural Conservation, and Evolution in Animals.International journal of molecular sciences · 2024Article
- The Relationship between Circadian Rhythm and Cancer Disease.International journal of molecular sciences · 2024Review
- Strategies that regulate LSD1 for novel therapeutics.Acta pharmaceutica Sinica. B · 2024Review
- The Effect of Sargassum Angustifolium-derived AgNPs on Apoptosis-associated Genes in Acute Lymphoblastic Leukemia Cells.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Elraglusib (formerly 9-ING-41) possesses potent anti-lymphoma properties which cannot be attributed to GSK3 inhibition.Cell communication and signaling : CCS · 2023Article
- Review
- Article
- Cyclin-dependent kinase 7/9 inhibitor SNS-032 induces apoptosis in diffuse large B-cell lymphoma cells.Cancer biology & therapy · 2022Article
- The targets of aspirin in bladder cancer: bioinformatics analysis.BMC urology · 2022Article
- Protective effect of cilostazol and verapamil against thioacetamide-induced hepatotoxicity in rats may involve Nrf2/GSK-3β/NF-κB signaling pathway.Toxicology research · 2022Article
- GSK3β is a critical, druggable component of the network regulating the active NOTCH1 protein and cell viability in CLL.Cell death & disease · 2022Article
43 more citing papers are in PubMed but not listed here.
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 1 country.
Funding
Abstract
Chronic lymphocytic leukemia (CLL) is commonly defined as a disease of failed apoptosis of B cells and remains an incurable disease. The mechanism of resistance to apoptosis in CLL is complex and influenced by numerous factors, including nuclear factor kappaB (NFkappaB)-mediated expression of antiapoptotic molecules. Recent evidence indicates that glycogen synthase kinase-3beta (GSK-3beta) positively regulates NFkappaB-mediated gene transcription and cell survival. Using malignant B cells collected from patients with CLL, we find that both GSK-3beta and NFkappaB accumulate in the nucleus of CLL B cells, and pharmacologic inhibition of GSK-3 results in decreased expression of two NFkappaB target genes Bcl-2 and XIAP and a subsequent increase in CLL B-cell apoptosis ex vivo. Furthermore, we observed that inhibition of GSK-3 leads to a decrease in NFkappaB-mediated gene transcription but does not affect the nuclear accumulation of NFkappaB in CLL B cells. Last, using chromatin immunoprecipitation, we show that GSK-3 inhibition abrogates NFkappaB binding to its target gene promoters (XIAP, Bcl-2), in part through epigenetic modification of histones. Our results establish that inhibition of GSK-3 abrogates NFkappaB binding to its target gene promoters through an epigenetic mechanism, enhances apoptosis in CLL B cells ex vivo and identifies GSK-3 as a potential therapeutic target in the treatment of CLL.
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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.