GSK3 is a regulator of RAR-mediated differentiation
Open accessAbstract
Acute myeloid leukemia (AML) is the most common form of leukemia in adults. Unfortunately, the standard therapeutic agents used for this disease have high toxicities and poor efficacy. The one exception to these poor outcomes is the use of the retinoid, all-trans retinoic acid (ATRA), for a rare subtype of AML (APL). The use of the differentiation agent, ATRA, in combination with low-dose chemotherapy leads to the long-term survival and presumed cure of 75-85% of patients. Unfortunately ATRA has not been clinically useful for other subtypes of AML. Though many non-APL leukemic cells respond to ATRA, they require significantly higher concentrations of ATRA for effective differentiation. Here we show that the combination of ATRA with glycogen synthase kinase 3 (GSK3) inhibition significantly enhances ATRA-mediated AML differentiation and growth inhibition. These studies have revealed that ATRA's receptor, the retinoic acid receptor (RAR), is a novel target of GSK3 phosphorylation and that GSK3 can impact the expression and transcriptional activity of the RAR. Overall, our studies suggest the clinical potential of ATRA and GSK3 inhibition for AML and provide a mechanistic framework to explain the promising activity of this combination regimen.
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GSK3β inhibition promotes myeloid differentiation and apoptosis in leukemia cells.
“GSK3b inhibition promotes myeloid differentiation and apoptosis in leukemia cells (27)(28)(29)(30); however, mechanisms underlying GSK3b inhibition leading to myeloid differentiation are poorly understood.”
From FBW7 Inhibits Myeloid Differentiation in Acute Myeloid Leukemia via GSK3-Dependent Ubiquitination of PU.1 (2021) · cites this paper as [28]
The Results sections on AML differentiation and genetic evidence report that GSK3 inhibition promotes myeloid differentiation and that GSK3β knockdown increases differentiation. The Results section on AML growth reports growth inhibition, not apoptosis; the copy does not establish the apoptosis part of the claim. No page numbers are available in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredGSK3b negatively impacts expression and transcriptional activity of retinoic acid receptor by phosphorylating it at Ser445, so GSK3 inhibition promotes myeloid differentiation.
“Gupta and colleagues demonstrated that GSK3b negatively impacted expression and transcriptional activity of ATRA's receptor, the retinoic acid receptor by phosphorylating it at Ser445, hence GSK3 inhibition promoted myeloid differentiation (28).”
From FBW7 Inhibits Myeloid Differentiation in Acute Myeloid Leukemia via GSK3-Dependent Ubiquitination of PU.1 (2021) · cites this paper as [28]
The Results section (‘GSK3 modulates RAR expression and activity’; page unavailable) shows that GSK3β phosphorylates RARα at Ser445, that GSK3 inhibition increases RAR expression and transcriptional activity, and that a S443A/S445A mutant has increased RAR levels. Another Results section (‘GSK3 inhibition alone induces moderate AML differentiation’; page unavailable) reports differentiation after GSK3 inhibition. The paper does not establish that phosphorylation at Ser445 alone causes both the reduced expression and reduced transcriptional activity asserted in the sentence. (LLM, conf=0.86)
Experimental — accuracy not yet measured
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- Authors
- Gupta, K., Gulen, F., Sun, L., Aguilera, R., Chakrabarti, A., Kiselar, J., Agarwal, M. K., & Wald, D. N.
- Affiliations
- Case Western Reserve University (US)
- Corresponding author
- Wald, D N
- Venue
- Leukemia
- Published
- 2012-01-06
- Volume
- 26
- Issue
- 6
- Pages
- 1277-1285
- ISSN
- 0887-6924 (ISSN-L)
- 1476-5551
- PMC
- PMC4458365
- OpenAlex
- W1992861698
- Cited by
- 50
- References
- 29
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 1 · 2023: 4 · 2022: 4 · 2021: 3 · 2020: 7 · 2019: 2 · 2018: 6 · 2017: 2 · 2016: 4 · 2015: 6 · 2014: 4 · 2013: 2 · 2012: 2
- FWCI
- 1.80
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Leukemia (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (UL1TR000439)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Keywords
- glycogen synthase kinase-3, retinoic acid receptor, all-trans retinoic acid, acute myeloid leukemia, leukemia cell differentiation, GSK3 phosphorylation, combination therapy, transcriptional regulation, leukemia cell growth inhibition
- MeSH terms
- Animals, Antineoplastic Agents, Cell Differentiation, Cells, Cultured, Drug Synergism, Enzyme Inhibitors, Female, Humans, Luciferases, Mice, Nude, Phosphorylation, RNA, Messenger, Tretinoin, Blotting, Western, Leukemia, Myeloid, Acute, Transcriptional Activation, Receptors, Retinoic Acid, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization, Glycogen Synthase Kinase 3, Immunoprecipitation, Mice, Real-Time Polymerase Chain Reaction
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Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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