Cited by 269Acute Lymphoblastic Leukemia researchWnt/β-catenin signaling in development and cancerAcute Myeloid Leukemia Research

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Glycogen synthase kinase 3 in MLL leukaemia maintenance and targeted therapy

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Wang, Zhong, Smith, Kevin S., Murphy, Mark, Piloto, Obdulio, Somervaille, Tim C. P., Cleary, Michael L.·2008·Nature

DOI 10.1038/nature07284PMC PMC4084721

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Abstract

Glycogen synthase kinase 3 (GSK3) is a multifunctional serine/threonine kinase that participates in numerous signalling pathways involved in diverse physiological processes. Several of these pathways are implicated in disease pathogenesis, which has prompted efforts to develop GSK3-specific inhibitors for therapeutic applications. However, before now, there has been no strong rationale for targeting GSK3 in malignancies. Here we report pharmacological, physiological and genetic studies that demonstrate an oncogenic requirement for GSK3 in the maintenance of a specific subtype of poor prognosis human leukaemia, genetically defined by mutations of the MLL proto-oncogene. In contrast to its previously characterized roles in suppression of neoplasia-associated signalling pathways, GSK3 paradoxically supports MLL leukaemia cell proliferation and transformation by a mechanism that ultimately involves destabilization of the cyclin-dependent kinase inhibitor p27(Kip1). Inhibition of GSK3 in a preclinical murine model of MLL leukaemia provides promising evidence of efficacy and earmarks GSK3 as a candidate cancer drug target.

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Authors: Wang, Z., Smith, K. S., Murphy, M., Piloto, O., Somervaille, T. C. P., & Cleary, M. L.
Affiliations: Stanford Medicine (US)
Corresponding author: Cleary, Michael L.
ORCID: Wang, Zhong
Smith, Kevin S.
Murphy, Mark
Somervaille, Tim C. P.
Cleary, Michael L.
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 2008-09-17
Volume: 455
Issue: 7217
Pages: 1205-1209
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/nature07284
PMC: PMC4084721
OpenAlex: W1964632863
Cited by: 265
References: 43
Citations by year: 2026: 3 · 2025: 6 · 2024: 6 · 2023: 8 · 2022: 9 · 2021: 10 · 2020: 17 · 2019: 14 · 2018: 13 · 2017: 13 · 2016: 14 · 2015: 14 · 2014: 23 · 2013: 29 · 2012: 26
FWCI: 19.78
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
RePEc: Research Papers in Economics (submittedVersion)
Funders: David and Lucile Packard Foundation
Lawrence Foundation
National Cancer Institute (CA 116606, R01CA116606, CA-55029, R01CA055029)
Topics: Health Sciences › Medicine › Hematology › Acute Lymphoblastic Leukemia research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
Keywords: glycogen synthase kinase-3, p27, cyclin-dependent kinase inhibitors, GSK-3 inhibitors, oncogenic signaling, therapeutic target
MeSH terms: Proto-Oncogene Mas, Animals, Cell Division, Cell Line, Transformed, Cell Transformation, Neoplastic, Disease Models, Animal, Humans, Isoenzymes, Leukemia, Lymphoid, Mice, Inbred C57BL, Histone-Lysine N-Methyltransferase, G1 Phase, Mice, SCID, Myeloid Progenitor Cells, Glycogen Synthase Kinase 3, Cell Line, Tumor, Intracellular Signaling Peptides and Proteins, Cell Proliferation, Cyclin-Dependent Kinase Inhibitor p27, Mice, Myeloid-Lymphoid Leukemia Protein, Precursor Cells, B-Lymphoid

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Glycogen synthase kinase 3 in MLL leukaemia maintenance and targeted therapy

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