Downregulation of Mcl-1 through GSK-3β activation contributes to arsenic trioxide-induced apoptosis in acute myeloid leukemia cells
Open accessAbstract
Arsenic trioxide (ATO) induces disease remission in acute promyelocytic leukemia (APL) patients, but not in non-APL acute myeloid leukemia (AML) patients. ATO at therapeutic concentrations (1-2 μM) induces APL NB4, but not non-APL HL-60, cells to undergo apoptosis through the mitochondrial pathway. The role of antiapoptotic protein Mcl-1 in ATO-induced apoptosis was determined. The levels of Mcl-1 were decreased in NB4, but not in HL-60, cells after ATO treatment through proteasomal degradation. Both glycogen synthase kinase-3β (GSK-3β) inhibitor SB216763 and siRNA blocked ATO-induced Mcl-1 reduction as well as attenuated ATO-induced apoptosis in NB4 cells. Silencing Mcl-1 sensitized HL-60 cells to ATO-induced apoptosis. Both ERK and AKT inhibitors decreased Mcl-1 levels and enhanced ATO-induced apoptosis in HL-60 cells. Sorafenib, an Raf inhibitor, activated GSK-3β by inhibiting its phosphorylation, decreased Mcl-1 levels and decreased intracellular glutathione levels in HL-60 cells. Sorafenib plus ATO augmented reactive oxygen species production and apoptosis induction in HL-60 cells and in primary AML cells. These results indicate that ATO induces Mcl-1 degradation through activation of GSK-3β in APL cells and provide a rationale for utilizing ATO in combination with sorafenib for the treatment of non-APL AML patients.
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GSK3β phosphorylation and subsequent proteasomal degradation of MCL-1 mediate cell death triggered by GSK3β activation.
“Phosphorylation by GSK3 b and subsequently enhanced proteasomal degradation of MCL-1, a pro-survival member of the BCL-2 family of proteins, mediates cell death triggered by GSK3 b activation (Maurer et al., 2006; Wang et al., 2012).”
From Combination of Hypoglycemia and Metformin Impairs Tumor Metabolic Plasticity and Growth by Modulating the PP2A-GSK3β-MCL-1 Axis (2019) · cites this paper as Wang et al., 2012
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Wired to Survive: How AML Cytogenetics Shape Apoptotic Dependence and Venetoclax Resistance
Rojas, A., Jethi, S., Budak-Alpdoǧan, T., & Pandey, M. K. (2026) · Genes · doi:10.3390/genes17091122
- Authors
- Wang, R., Xia, L., Gabrilove, J., Waxman, S., & Jing, Y.
- Affiliations
- Tisch Cancer Institute (US)
- Corresponding author
- Jing, Y
- Venue
- Leukemia
- Published
- 2012-07-03
- Volume
- 27
- Issue
- 2
- Pages
- 315-324
- ISSN
- 0887-6924 (ISSN-L)
- 1476-5551
- PMC
- PMC3478411
- OpenAlex
- W2013966534
- Cited by
- 85
- References
- 57
- Citations by year
- 2026: 1 · 2025: 7 · 2024: 3 · 2023: 4 · 2022: 8 · 2021: 11 · 2020: 7 · 2019: 5 · 2018: 6 · 2017: 2 · 2016: 4 · 2015: 13 · 2014: 8 · 2013: 4 · 2012: 2
- FWCI
- 3.45
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Leukemia (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (R01CA093533)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Keywords
- arsenic trioxide, Mcl-1, GSK3β, acute myeloid leukemia, acute promyelocytic leukemia, apoptosis, proteasomal degradation, mitochondrial apoptosis, sorafenib, ERK inhibition, AKT inhibition, glutathione, reactive oxygen species, combination therapy
- MeSH terms
- Glycogen Synthase Kinase 3 beta, Arsenic Trioxide, Antineoplastic Agents, Arsenicals, Enzyme Activation, Flow Cytometry, Glutathione, Humans, Mitochondria, Oxides, Phosphorylation, Tumor Cells, Cultured, Blotting, Western, Leukemia, Myeloid, Acute, Down-Regulation, Apoptosis, Reactive Oxygen Species, Proto-Oncogene Proteins c-bcl-2, RNA, Small Interfering, Glycogen Synthase Kinase 3, Myeloid Cell Leukemia Sequence 1 Protein
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