ArticleNature cell biology2024
SHP-1 inhibition targets leukaemia stem cells to restore immunosurveillance and enhance chemosensitivity by metabolic reprogramming.
Article in Nature cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Multidrug resistance in cancer: current understandings and future perspective.Molecular biomedicine · 2026Review
- Lactate metabolism and epigenetic reprogramming drive c-KIT hyperactivation to mediate Gilteritinib resistance: Rationale for c-KIT degraders over kinase inhibitors.Acta pharmaceutica Sinica. B · 2026Article
- From complexity to clarity: aging bone marrow niche in bone and blood regeneration and malignancy.Bone research · 2026Review
- The controversial role of metabolic reprogramming in anti-tumor therapy resistance.Discover oncology · 2026Review
- PFKP in malignant tumors: bridging metabolic reprogramming, post-translational modifications, and the immunosuppressive microenvironment.Frontiers in cell and developmental biology · 2026Review
- How to drug a leukemic stem cell: deciphering heterogeneity for better specificity.Blood neoplasia · 2025Review
- CPT2 inhibition enhances selective autophagy and proliferation in colorectal cancer via GPAT4-dependent glycerophospholipid biosynthesis.Communications biology · 2025Article
- BRG1 inhibits glycolysis by promoting SHP1-mediated dephosphorylation of PKM2 in non-small cell lung cancer.Oncogenesis · 2025Article
- Phosphofructokinase-1 redefined: a metabolic hub orchestrating cancer hallmarks through multi-dimensional control networks.Journal of translational medicine · 2025Review
- Targeting stem-property and vasculogenic mimicry for sensitizing paclitaxel therapy of triple-negative breast cancer by biomimetic codelivery.Acta pharmaceutica Sinica. B · 2025Article
- Article
- Overexpressing natural killer group 2 member A drives natural killer cell exhaustion in relapsed acute myeloid leukemia.Signal transduction and targeted therapy · 2025Article
- Warburg effect and lactylation in cancer: mechanisms for chemoresistance.Molecular medicine (Cambridge, Mass.) · 2025Review
- Metabolic Targeting of Oxidative Phosphorylation Enhances Chemosensitivity in Triple-Negative Breast Cancer via a Synergistic Nanomedicine.Theranostics · 2025Article
- Pioneering biomimetic biomaterial for leukemia therapy enhancement: a review.Frontiers in bioengineering and biotechnology · 2025Review
- Decoding CD24: Roles of chemoradiotherapy resistance and potential as therapeutic targets.Oncology research · 2025Review
- Metabolic reprogramming and immune regulation in acute myeloid leukemia.Frontiers in immunology · 2025Review
- Phase 1 study of chidamide in combination with venetoclax, azacitidine, aclarubicin, cytarabine and G-CSF for refractory/relapsed acute myeloid leukemia: clinical safety, efficacy, and correlative analysis.Frontiers in immunology · 2025Article
- Effects ofCurrent issues in molecular biology · 2024Article
- PPIC-labeled CAFs: Key players in neoadjuvant chemotherapy resistance for gastric cancer.Translational oncology · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
Abstract
Leukaemia stem cells (LSCs) in acute myeloid leukaemia present a considerable treatment challenge due to their resistance to chemotherapy and immunosurveillance. The connection between these properties in LSCs remains poorly understood. Here we demonstrate that inhibition of tyrosine phosphatase SHP-1 in LSCs increases their glycolysis and oxidative phosphorylation, enhancing their sensitivity to chemotherapy and vulnerability to immunosurveillance. Mechanistically, SHP-1 inhibition leads to the upregulation of phosphofructokinase platelet (PFKP) through the AKT-β-catenin pathway. The increase in PFKP elevates energy metabolic activities and, as a consequence, enhances the sensitivity of LSCs to chemotherapeutic agents. Moreover, the upregulation of PFKP promotes MYC degradation and, consequently, reduces the immune evasion abilities of LSCs. Overall, our study demonstrates that targeting SHP-1 disrupts the metabolic balance in LSCs, thereby increasing their vulnerability to chemotherapy and immunosurveillance. This approach offers a promising strategy to overcome LSC resistance in acute myeloid leukaemia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.