ArticleHaematologica2021
Targeting of plasminogen activator inhibitor-1 activity promotes elimination of chronic myeloid leukemia stem cells.
Article in Haematologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- Chronic myeloid leukemia in a global context: confirmatory findings and novel discoveries from a refined Japanese Cohort.Leukemia · 2026Review
- Diverse roles of SERPINE1 in regulating cellular proliferation and invasion.International journal of oncology · 2026Article
- Inflammatory macrophage-derived plasminogen activator inhibitor-1 exacerbates inflammation through efferocytosis inhibition.Cell death discovery · 2026Article
- Plasminogen Activator Inhibitor-1 Mediates Tolerance to Anti-PD-1 Immunotherapy in Non-Small Cell Lung Cancer.Molecular cancer therapeutics · 2026Article
- The structure and functions of TRAF families and recent advances of TRAFs in leukemia.Frontiers in oncology · 2026Review
- Dysregulation of MicroRNA-181a-5p Targets TNFAIP3 to Promote MIF-CXCR4 Signaling and Immune Inflammatory Remodeling in Chronic Myeloid Leukemia.F1000Research · 2025Article
- Review
- Plasminogen activator inhibitor-1 promotes immune evasion in tumors by facilitating the expression of programmed cell death-ligand 1.Frontiers in immunology · 2024Article
- miR-181a plays the tumor-suppressor role in chronic myeloid leukemia CD34Cellular and molecular life sciences : CMLS · 2023Article
- Translating Senotherapeutic Interventions into the Clinic with Emerging Proteomic Technologies.Biology · 2023Review
- Time to relapse in chronic lymphocytic leukemia and DNA-methylation-based biological age.Clinical epigenetics · 2023Article
- Deep molecular response in patients with chronic phase chronic myeloid leukemia treated with the plasminogen activator inhibitor-1 inhibitor TM5614 combined with a tyrosine kinase inhibitor.Cancer medicine · 2023Article
- Properties of Leukemic Stem Cells in Regulating Drug Resistance in Acute and Chronic Myeloid Leukemias.Biomedicines · 2022Review
- Stromal Factors as a Target for Immunotherapy in Melanoma and Non-Melanoma Skin Cancers.International journal of molecular sciences · 2022Review
- Chronic myeloid leukemia stem cells: targeting therapeutic implications.Stem cell research & therapy · 2021Review
- Pharmacological inhibition of PAI-1 alleviates cardiopulmonary pathologies induced by exposure to air pollutants PMEnvironmental pollution (Barking, Essex : 1987) · 2021Article
- Plasminogen Activating Inhibitor-1 Might Predict the Efficacy of Anti-PD1 Antibody in Advanced Melanoma Patients.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Therapeutic strategies that target leukemic stem cells (LSCs) provide potential advantages in the treatment of chronic myeloid leukemia (CML). Here, we show that selective blockade of plasminogen activator inhibitor-1 (PAI-1) enhances the susceptibility of CML-LSCs to tyrosine kinase inhibitor (TKI), which facilitates the eradication of CML-LSCs and leads to sustained remission of the disease. We demonstrated for the first time that TGF-β-PAI-1 axis was selectively augmented in CML-LSCs in the bone marrow (BM), whereby protecting CML-LSCs from TKI treatment. Furthermore, the combined administration of TKI plus a PAI-1 inhibitor, in a mouse model of CML, significantly enhanced the eradication of CML cells in the BM and prolonged the survival of CML mice. The combined therapy of imatinib and a PAI-1 inhibitor prevented the recurrence of CML-like disease in serially transplanted recipients, indicating the elimination of CML-LSCs. Interestingly, PAI-1 inhibitor treatment augmented membrane-type matrix metalloprotease-1 (MT1-MMP)-dependent motility of CML-LSCs, and the anti-CML effect of PAI-1 inhibitor was extinguished by the neutralizing antibody for MT1-MMP, underlining the mechanistic importance of MT1-MMP. Our findings provide evidence of, and a rationale for, a novel therapeutic tactic, based on the blockade of PAI-1 activity, for CML patients.
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Registered trials
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