ArticleHaematologica2019
The high NRF2 expression confers chemotherapy resistance partly through up-regulated DUSP1 in myelodysplastic syndromes.
Article in Haematologica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 48 citations in OpenAlex.
- NRF2 activation is required for chemotherapy resistance acquisition in medulloblastoma via metabolic and redox adaptation.Redox biology · 2026Article
- The Role of Iron-Overloaded Macrophages in Mesenchymal Stem Cell Senescence and Anemia in Myelodysplastic Syndromes: Protocol for an In Vitro Study.JMIR research protocols · 2026Article
- Review
- Review
- Inhibition of NRF2 signaling overcomes acquired resistance to arsenic trioxide in FLT3-mutated Acute Myeloid Leukemia.Annals of hematology · 2024Article
- Iron overload induces dysplastic erythropoiesis and features of myelodysplasia in Nrf2-deficient mice.Leukemia · 2024Article
- Immune checkpoints represent a promising breakthrough in targeted therapy and prognosis of myelodysplastic syndrome.Heliyon · 2023Review
- Targeted Silencing of NRF2 by rituximab-conjugated nanoparticles increases the sensitivity of chronic lymphoblastic leukemia cells to Cyclophosphamide.Cell communication and signaling : CCS · 2023Article
- All-trans retinoic acid enhances the cytotoxic effect of decitabine on myelodysplastic syndromes and acute myeloid leukaemia by activating the RARα-Nrf2 complex.British journal of cancer · 2023Article
- Nrf2 overexpression increases the resistance of acute myeloid leukemia to cytarabine by inhibiting replication factor C4.Cancer gene therapy · 2022Article
- 7-Antioxidants (Basel, Switzerland) · 2022Article
- Dual-specificity phosphatases: therapeutic targets in cancer therapy resistance.Journal of cancer research and clinical oncology · 2022Review
- Nrf2 Overexpression Decreases Vincristine Chemotherapy Sensitivity Through the PI3K-AKT Pathway in Adult B-Cell Acute Lymphoblastic Leukemia.Frontiers in oncology · 2022Article
- Impact of Nrf2 expression in reconstituting T-cells of allogeneic hematopoietic stem cell transplanted patients.Leukemia · 2021Article
- Nrf2 overexpression increases risk of high tumor mutation burden in acute myeloid leukemia by inhibiting MSH2.Cell death & disease · 2021Article
- Application Research of Individualized Conditional Reprogramming System to Guide Treatment of Gastric Cancer.Frontiers in oncology · 2021Article
- Article
- Oxidative Stress Parameters Can Predict the Response to Erythropoiesis-Stimulating Agents in Myelodysplastic Syndrome Patients.Frontiers in cell and developmental biology · 2021Article
- The NRF2, Thioredoxin, and Glutathione System in Tumorigenesis and Anticancer Therapies.Antioxidants (Basel, Switzerland) · 2020Review
- Nuclear Factor Erythroid 2-Related Factor 2 in Regulating Cancer Metabolism.Antioxidants & redox signaling · 2020Review
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Authors and funding
22 authors at 2 institutions in 2 countries.
Funding
Abstract
Although cytarabine has been widely considered as one of the chemotherapy drugs for high-risk myelodysplastic syndromes (MDS), the overall response rate is only approximately 20-30%. Nuclear factor erythroid 2-related factor 2 (NRF2, also called NFE2L2) has been shown to play a pivotal role in preventing cancer cells from being affected by chemotherapy. However, it is not yet known whether NRF2 can be used as a prognostic biomarker in MDS, or whether elevated NRF2 levels are associated with cytarabine resistance. Here, we found that NRF2 expression levels in bone marrow from high-risk patients exceeded that of low-risk MDS patients. Importantly, high NRF2 levels are correlated with inferior outcomes in MDS patients (n=137). Downregulation of NRF2 by the inhibitor Luteolin, or lentiviral shRNA knockdown, enhanced the chemotherapeutic efficacy of cytarabine, while MDS cells treated by NRF2 agonist Sulforaphane showed increased resistance to cytarabine. More importantly, pharmacological inhibition of NRF2 could sensitize primary high-risk MDS cells to cytarabine treatment. Mechanistically, downregulation of dual specificity protein phosphatase 1, an NRF2 direct target gene, could abrogate cytarabine resistance in NRF2 elevated MDS cells. Silencing NRF2 or dual specificity protein phosphatase 1 also significantly sensitized cytarabine treatment and inhibited tumors in MDS cells transplanted mouse models
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