ArticleBlood advances2023
FOXP1 regulates oxidative stress, SIRT1 expression, and resistance to chemotherapies in acute myeloid leukemia cells.
Article in Blood advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- SIRT1 in Senescence: Mitochondria and Immune Crosstalk.Biology · 2026Review
- Optical Genome Mapping Reveals Frequent Cryptic Structural Aberrations in Normal Karyotype Acute Myeloid Leukemia.International journal of cancer · 2026Article
- Antileukemic Potential of Sodium Caseinate in Cytarabine-Resistant HL60-CR50 Human Leukemia Cells.Molecules (Basel, Switzerland) · 2025Article
- SIRT1 as a masterful reciprocal regulator of molecular mechanisms and signaling pathways involved in tumor growth and expansion.Clinical and experimental medicine · 2025Review
- High Burden of Non-Clonal Chromosome Aberrations Before Onset of Detectable Neoplasia in Fanconi Anemia Bone Marrow.Cancers · 2025Article
- The Role of the Sirtuin Family Histone Deacetylases in Acute Myeloid Leukemia-A Promising Road Ahead.Cancers · 2025Review
- Targeting FOXP1 phase separation in small cell lung cancer mechanisms of chemotherapy resistance.Communications biology · 2025Article
- Harnessing the FOXO-SIRT1 axis: insights into cellular stress, metabolism, and aging.Biogerontology · 2025Review
- FOXP1 is associated with oncogenesis and clinical outcomes in hematologic malignancies.Frontiers in immunology · 2025Article
- The Role of SIRT1 in Leukemia.Current treatment options in oncology · 2024Review
- Comprehensive pan-cancer analysis reveals SIRT5 is a predictive biomarker for prognosis and immunotherapy response.Functional & integrative genomics · 2024Article
- Acute myeloid leukemia with unreported translocation (x; 3) (q24; p13): A case report.Clinical case reports · 2024Article
- Integrative alternative splicing analysis reveals new prognosis signature in B-cell acute lymphoblastic leukemia.International journal of biological sciences · 2024Article
- Reactive oxygen species and its role in pathogenesis and resistance to therapy in acute myeloid leukemia.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Role of SIRT1 in Chemoresistant Leukemia.International journal of molecular sciences · 2023Review
- The Critical Role of Sirt1 in Subarachnoid Hemorrhages: Mechanism and Therapeutic Considerations.Brain sciences · 2023Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcription factor Forkhead box P1 (FOXP1) belongs to the same protein family as the FOXOs that are well-known regulators of murine hematopoietic stem progenitor cell (HSPC) maintenance via dampening oxidative stress. FOXP1 and FOXOs can play opposite, or similar, roles depending on cell context; they can crossregulate each other's expression. In a previous study, we have shown that FOXP1 contributes to healthy human HSPC and acute myeloid leukemia (AML) cell growth. Here, we investigated the role of FOXP1 in HSPCs and AML cell oxidative stress defense in a human context. FOXP1 expression level was associated with an inferior survival outcome in patients with cytogenetically normal AML. FOXP1 knockdown enhanced superoxide anion levels of human-committed CD34+CD38+ cells but not stem cell-enriched CD34+CD38- HSPCs or AML cells in vitro. FOXP1 knockdown triggered enhanced NRF2 activity and increased cell oxidative stress. FOXP1 had no impact on FOXO1/3/4 expression in these cells; genetic and pharmacological inhibition of FOXOs did not change superoxide anion levels of human HSPCs or AML cells. Moreover, FOXP1 antioxidant activity was independent of changes in expression of superoxide dismutase 1 and 2 or catalase. Instead, FOXP1 upregulated expression of the stress sensor SIRT1 by stabilizing SIRT1 protein. FOXP1 loss sensitized AML cells to chemotherapy. Together, this study identified FOXP1 as a new safeguard against myeloid progenitor oxidative stress, which works independently of FOXOs but through SIRT1 and contributes to AML chemoresistance. It proposes FOXP1 expression/activity as a promising target to overcome drug resistance of AML HSPCs.
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