NDLI: Neutrophil elastase enhances the proliferation and decreases apoptosis of leukemia cells via activation of PI3K/Akt signaling

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Neutrophil elastase enhances the proliferation and decreases apoptosis of leukemia cells via activation of PI3K/Akt signaling

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Neutrophil elastase enhances the proliferation and decreases apoptosis of leukemia cells via activation of PI3K/Akt signaling

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Jiang, Kai-Ling Yang, Rong Song, Hao Yang, Xiao-Qun Li, Liu Zhong, Liang Liu, Bei-Zhong
Description	Author Affiliation: Yang R ( Central Laboratory of YongChuan Hospital, Chongqing Medical University, Chongqing 402160, P.R. China.); Zhong L ( Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, P.R. China.); Yang XQ ( Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, P.R. China.); Jiang KL ( Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, P.R. China.); Li L ( Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, P.R. China.); Song H ( Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, P.R. China.); Liu BZ ( Central Laboratory of YongChuan Hospital, Chongqing Medical University, Chongqing 402160, P.R. China.)
Abstract	Neutrophil elastase (NE) is a neutrophilderived 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 promyelocyte retinoic acid receptoralpha chimeric protein and is important for the development of acute promyelocytic leukemia. To further elucidate the role of NE in acute promyelocytic leukemia, the present study successfully constructed a lentiviral vector containing the NE gene (LV5NE), which was transfected into NB4 acute promyelocytic leukemia cells. The effects of NE overexpression in NB4 cells were detected using a Cell-Counting Kit8 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 promyelocytic leukemia.
ISSN	17912997
e-ISSN	17913004
DOI	10.3892/mmr.2016.5051
Journal	Molecular Medicine Reports
Issue Number	5
Volume Number	13
Language	English
Publisher	Spandidos Publications
Publisher Date	2016-05-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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