Inhibition of NRF2 enhances the acute myeloid leukemia cell death induced by venetoclax via the ferroptosis pathway
Open accessAbstract
Venetoclax, an inhibitor that selectively targets B cell lymphoma-2 (BCL-2) that has been approved for treating adult acute myeloid leukemia (AML) in combination with hypomethylating agents. However, its short duration of response and emergence of resistance are significant issues. In this study, we found that the sensitivity of AML cells to venetoclax was considerably enhanced by ML385, an inhibitor of the ferroptosis factor nuclear transcription factor erythroid 2-related factor 2 (NRF2). Using AML samples, we verified that NRF2 and its target gene ferritin heavy chain 1 (FTH1) were highly expressed in patients with AML and correlated with poor prognosis. Downregulation of NRF2 could inhibit FTH1 expression and significantly enhance the venetoclax-induced labile iron pool and lipid peroxidation. By contrast, NRF2 overexpression or administration of the reactive oxygen species inhibitor N-acetylcysteine and vitamin E could effectively suppress the anti-AML effects of ML385+venetoclax. Furthermore, the ferroptosis inducer erastin increased the anti-AML effects of venetoclax. Our study demonstrated that NRF2 inhibition could enhance the AML cell death induced by venetoclax via the ferroptosis pathway. Thus, the combination of ML385 with venetoclax may offer a favorable strategy for AML treatment.
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All ApoE isoforms increased the expression of known NRF2 target genes including SLC7A11, AKR1C1, and FTH1.
“and increased the expression of known target genes of this transcription factor including SLC7A11, AKR1C1, and FTH1 (fig. S5S) (41–45).”
From Secreted Apoe rewires melanoma cell state vulnerability to ferroptosis (2024) · cites this paper as [42]
The Introduction identifies SLC7A11 and FTH1 as well-defined NRF2 target genes, and the Results report that NRF2 overexpression promotes their expression in AML cells. Our copy does not identify AKR1C1 as an NRF2 target. The ApoE-isoform expression finding is presented as the citing paper’s own result (fig. S5S), not as a finding of this source. (LLM, conf=0.86)
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- Authors
- Yu, X., Wang, Y., Tan, J., Li, Y., Yang, P., Liu, X., Lai, J., Zhang, Y., Cai, L., Gu, Y., Xu, L., & Li, Y.
- Affiliations
- Jinan University (CN)
- Corresponding author
- Xu, Ling
- Li, Yangqiu
- ORCID
- Venue
- Cell Death Discovery
- Published
- 2024-01-18
- Volume
- 10
- Issue
- 1
- Pages
- 35-35
- ISSN
- 2058-7716 (ISSN-L)
- PMC
- PMC10796764
- OpenAlex
- W4390984730
- Cited by
- 48
- References
- 59
- Citations by year
- 2026: 17 · 2025: 23 · 2024: 8
- FWCI
- 14.89
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Cell Death Discovery (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (82000108, 82200167)
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Ferroptosis and cancer prognosis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
- Keywords
- acute myeloid leukemia, venetoclax, Nrf2 inhibition, ML385, ferroptosis, FTH1, labile iron pool, lipid peroxidation, BCL-2 inhibitor, combination therapy, erastin, reactive oxygen species, N-acetylcysteine, vitamin E, drug resistance
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