ArticleMolecular medicine reports2016
Neutrophil elastase enhances the proliferation and decreases apoptosis of leukemia cells via activation of PI3K/Akt signaling.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.
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Who cites it
19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 28 citations in OpenAlex.
- Prognostic value of baseline LIPI, LDH and dNLR in ES-SCLC patients receiving immune checkpoint inhibitors: a systematic review and meta-analysis.Frontiers in immunology · 2025Pooled it
- Prognostic value of lung immune prognostic index in non-small cell lung cancer patients receiving immune checkpoint inhibitors: a meta-analysis.Pathology oncology research : POR · 2024Pooled it
- Neutrophil extracellular traps induce chemoresistance in human breast cancer cells through the PI3K/AKT/NF-κB pathway.Frontiers in immunology · 2026Article
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- 3D DNAzyme Motor Nanodevice With Self-Powered FRET Amplifier and Self-Supplied HAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- Exploiting innate immunity for cancer immunotherapy.Molecular cancer · 2023Review
- Tumor-associated neutrophils in pancreatic cancer progression and metastasis.American journal of cancer research · 2023Review
- Neutrophils in cancer carcinogenesis and metastasis.Journal of hematology & oncology · 2021Review
- Human Antibody Domains and Fragments Targeting Neutrophil Elastase as Candidate Therapeutics for Cancer and Inflammation-Related Diseases.International journal of molecular sciences · 2021Article
- Coagulopathy in Acute Promyelocytic Leukemia: Can We Go Beyond Supportive Care?Frontiers in medicine · 2021Review
- Neutrophils in the Tumor Microenvironment.Advances in experimental medicine and biology · 2020Review
- microRNA-146a Promotes Growth of Acute Leukemia Cells by Downregulating Ciliary Neurotrophic Factor Receptor and Activating JAK2/STAT3 Signaling.Yonsei medical journal · 2019Article
- Tumor-Associated Neutrophils in Cancer: Going Pro.Cancers · 2019Review
- Silencing theYonsei medical journal · 2019Article
- Luteolin Partially Inhibits LFA-1 Expression in Neutrophils Through the ERK Pathway.Inflammation · 2019Article
- Cxcr1 mediates recruitment of neutrophils and supports proliferation of tumor-initiating astrocytes in vivo.Scientific reports · 2018Article
- Location of NLS-RARα protein in NB4 cell and nude mice.Oncology letters · 2017Article
- Ze-qi Decoction Inhibits Neutrophil Extracellular Trap Formation to Suppress the Progression and Metastasis of Non-Small Cell Lung Cancer.Integrative cancer therapiesArticle
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophil elastase (NE) is a neutrophil‑derived serine proteinase with specificity for a broad range of substrates. NE has been reported to be associated with the pathogenesis of several conditions, particularly that of pulmonary diseases. Previous studies have shown that NE can cleave the pro‑myelocyte ‑ retinoic acid receptor‑alpha chimeric protein and is important for the development of acute pro‑myelocytic leukemia. To further elucidate the role of NE in acute pro‑myelocytic leukemia, the present study successfully constructed a lentiviral vector containing the NE gene (LV5‑NE), which was transfected into NB4 acute pro‑myelocytic leukemia cells. The effects of NE overexpression in NB4 cells were detected using a Cell-Counting Kit‑8 assay, flow cytometry and western blot analysis. The results showed that NE significantly promoted the proliferation of NB4 cells, inhibited cell apoptosis and apoptotic signaling, and led the activation of Akt. In an additional experiment, a vector expressing small hairpin RNA targeting NE was constructed to assess the effects of NE knockdown in U937 cells. Western blot analysis revealed that apoptotic signaling was increased, while Akt activation was decreased following silencing of NE. The results of the present study may indicate that NE activates the phosphoinositide-3 kinase/Akt signaling pathway in leukemia cells to inhibit apoptosis and enhance cell proliferation, and may therefore represent a molecular target for the treatment of pro‑myelocytic leukemia.
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