Therapeutic targeting of TP53-mutated acute myeloid leukemia by inhibiting HIF-1α with echinomycin
Open accessAbstract
TP53 mutation in acute myeloid leukemia (AML) is associated with poor prognosis. Since no targeted therapy is available to restore p53 function, it is of great interest to test whether other pathways activated by TP53 mutations can be therapeutically targeted. Here, we showed HIF-1α target genes are enriched in TP53-mutated versus TP53-wild-type AML. To determine the role of this activation, we tested efficacy of HIF-1α inhibitor echinomycin in TP53-mutated AML samples in vitro and in vivo. Echinomycin was broadly effective against a panel of primary AML blast cells, with low nanomolar IC 50 s and, based on colony-forming unit assay, was tenfold more effective in eliminating AML stem cells. Echinomycin selectively eliminated CD34+CD38- AML cells. To test the therapeutic efficacy of echinomycin, we established a xenograft model of TP53-mutated AML. Echinomycin was broadly effective against xenografts from multiple AML samples in vivo, and more effective than cytarabine + daunorubicin chemotherapy. Importantly, while cytarabine + daunorubicin enriched for AML stem cells, echinomycin nearly eliminated this population. Using TP53-mutated AML cell line THP1 and patient-derived AML cells, we tested a new echinomycin formulation with longer half-life and significantly improved therapeutic effect. Our data suggest a novel approach to treat AML with TP53 mutations.
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Liposomal formulation increased the systemic exposure of echinomycin in the blood circulation.
“We have recently reported that liposomal formulation increased the systemic exposure of Echinomycin in the blood circulation36.”
From Liposomal Formulation of HIF-1α Inhibitor Echinomycin Eliminates Established Metastases of Triple-negative Breast Cancer (2020) · cites this paper as [36]
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Self-citation
- Authors
- Wang, Y., Liu, Y., Bailey, C., Zhang, H., He, M., Sun, D., Zhang, P., Parkin, B., Baer, M. R., Zheng, P., Malek, S. N., & Liu, Y.
- Affiliations
- University of Maryland, Baltimore (US)
- University of Michigan (US)
- Corresponding author
- Wang, Yin
- Liu, Yang
- ORCID
- Venue
- Oncogene
- Published
- 2020-02-15
- Volume
- 39
- Issue
- 14
- Pages
- 3015-3027
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- PMC
- PMC7291851
- OpenAlex
- W3006455792
- Cited by
- 38
- References
- 33
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 5 · 2023: 7 · 2022: 7 · 2021: 7 · 2020: 4
- FWCI
- 3.95
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Health & Human Services | NIH | National Cancer Institute (CA164469, CA171972, CA183030)
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- TP53 mutation, acute myeloid leukemia, HIF-1α inhibition, echinomycin, CD34+CD38- cells, xenograft models, targeted therapy, drug formulation
- MeSH terms
- Animals, Echinomycin, Female, Humans, Male, Mutation, Leukemia, Myeloid, Acute, Tumor Suppressor Protein p53, Apoptosis, Cell Line, Tumor, Mice, Hypoxia-Inducible Factor 1, alpha Subunit
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