GSK-3 inhibition sensitizes acute myeloid leukemia cells to 1,25D-mediated differentiation
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Abstract
1,25-dihydroxyvitamin D3 (1,25D), the biologically active form of vitamin D, is widely considered a promising therapy for acute myeloid leukemia (AML) based on its ability to drive differentiation of leukemic cells. However, clinical trials have been disappointing in part to dose-limiting hypercalcemia. Here we show how inhibiting glycogen synthase kinase 3 (GSK3) can improve the differentiation response of AML cells to 1,25D-mediated differentiation. GSK3 inhibition in AML cells enhanced the differentiating effects of low concentrations of 1,25D. In addition, GSK3 inhibition augmented the ability of 1,25D to induce irreversible growth inhibition and slow the progression of AML in mouse models. Mechanistic studies revealed that GSK3 inhibition led to the hyperphosphorylation of the vitamin D receptor (VDR), enabling an interaction between VDR and the coactivator, SRC-3 (NCOA3), thereby increasing transcriptional activity. We also found that activation of JNK-mediated pathways in response to GSK3 inhibition contributed to the potentiation of 1,25D-induced differentiation. Taken together, our findings offer a preclinical rationale to explore the repositioning of GSK3 inhibitors to enhance differentiation-based therapy for AML treatment. Cancer Res; 76(9); 2743-53. ©2016 AACR.
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GSK3b inhibition sensitizes AML cells to ATRA and to 1,25 vitamin D-mediated differentiation.
“While GSK3b inhibition was independently shown to sensitize AML cells to ATRA (48) as well 1,25 vitamin D-mediated differentiation (30), the underlying molecular mechanism remained unknown.”
From FBW7 Inhibits Myeloid Differentiation in Acute Myeloid Leukemia via GSK3-Dependent Ubiquitination of PU.1 (2021) · cites this paper as [30]
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- Authors
- Gupta, K., Stefan, T., Ignatz-Hoover, J., Moreton, S., Parizher, G., Saunthararajah, Y., & Wald, D. N.
- Affiliations
- Case Western Reserve University (US)
- Cleveland Clinic (US)
- University Hospitals of Cleveland (US)
- Corresponding author
- Wald, David N.
- Venue
- Cancer Research
- Published
- 2016-05-01
- Volume
- 76
- Issue
- 9
- Pages
- 2743-2753
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- PMC
- PMC5563074
- OpenAlex
- W2296231904
- Cited by
- 44
- References
- 35
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 2 · 2023: 6 · 2022: 2 · 2021: 4 · 2020: 11 · 2019: 1 · 2018: 6 · 2017: 5 · 2016: 4
- FWCI
- 4.84
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (F30CA186466)
- National Institute of General Medical Sciences (T32GM007250)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Vitamin D Research Studies
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Keywords
- acute myeloid leukemia, GSK3 inhibition, 1,25-dihydroxyvitamin D3, vitamin D receptor, differentiation therapy, hypercalcemia, SRC-3, NCOA3, JNK signaling, drug repurposing, leukemia progression
- MeSH terms
- Animals, Antineoplastic Combined Chemotherapy Protocols, Calcitriol, Cell Differentiation, Enzyme Inhibitors, Flow Cytometry, Humans, Phosphorylation, Blotting, Western, Signal Transduction, Leukemia, Myeloid, Acute, Receptors, Calcitriol, Oligonucleotide Array Sequence Analysis, Xenograft Model Antitumor Assays, Electrophoretic Mobility Shift Assay, Glycogen Synthase Kinase 3, Immunoprecipitation, Mice, Gene Knockdown Techniques, Nuclear Receptor Coactivator 3, Real-Time Polymerase Chain Reaction
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