Evidence map›Paper›PMID 26081156›Full record

ArticleMolecular medicine reports2015

Neutrophil elastase and its therapeutic effect on leukemia cells.

Kai-Ling Jiang, Peng-Peng Ma, Xiao-Qun Yang, Liang Zhong, Hui Wang, Xin-Yu Zhu, Bei-Zhong Liu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.4field-weighted citation impact, top 38% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 15 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Kai-Ling JiangCentral Laboratory of Yong‑Chuan Hospital, Chongqing Medical University, Chongqing 402160, P.R. China.
Peng-Peng MaCentral Laboratory of Yong‑Chuan Hospital, Chongqing Medical University, Chongqing 402160, P.R. China.
Xiao-Qun YangKey Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, P.R. China.
Liang ZhongKey Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, P.R. China.
Hui WangKey Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, P.R. China.
Xin-Yu ZhuKey Laboratory of Laboratory Medical Diagnostics, Ministry of Education, Department of Laboratory Medicine, Chongqing Medical University, Chongqing 400016, P.R. China.
Bei-Zhong LiuCentral Laboratory of Yong‑Chuan Hospital, Chongqing Medical University, Chongqing 402160, P.R. China.
Chongqing Medical University · CNChildren's Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophil elastase (NE) is an early myeloid-specific serine protease, which is predominantly produced by promyelocytes. A previous study demonstrated that NE has an important role in the development of acute promyelocytic leukemia (APL). The process of APL was shown to be accelerated in animals that expressed abundant NE, whereas NE‑deficient mice were protected from APL development; thus suggesting an important role for NE in the development of APL. The present study aimed to investigate the effects and possible mechanisms of NE. Up- and downregulation of NE in various leukemia cell lines was conducted in order to explore its significance in the occurrence and procession of leukemia, with the aim of identifying novel targeted therapeutic drugs for the treatment of leukemia. NE was overexpressed in cells following infection with an adenovirus, and Cell Counting kit‑8 and flow cytometry results demonstrated that cell proliferation was promoted, and cell apoptosis was inhibited, as compared with the untreated cells. NE was downregulated in the cells by both RNA interference and treatment with GW311616A, a specific inhibitor of NE, following which cell growth was shown to be inhibited and apoptosis was induced. These results suggested that NE may promote the development of APL, therefore, NE may be a therapeutic target and its inhibitor GW311616A may be a potential therapeutic drug for leukemia. Furthermore, the apoptosis‑associated protein B‑cell lymphoma 2 (Bcl‑2)‑associated X protein was significantly increased, whereas Bcl‑2 was markedly decreased in the cells with downregulated NE. Further experiments revealed that the probable apoptosis‑associated signaling pathway was the phosphoinositide 3‑kinase/AKT pathway. The present study is the first, to the best of our knowledge, to demonstrate that GW311616A, a specific NE inhibitor, may act as a potential targeted drug for leukemia, which may have a profound impact on the future of leukemia-targeted therapy.

Indexed as

Apoptosisbcl-2-Associated X ProteinCell Line, TumorCell ProliferationDown-RegulationHumansK562 CellsLeukemia, Promyelocytic, AcuteLeukocyte ElastasePhosphatidylinositol 3-KinasesPiperidinesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2RNA InterferenceRNA, Small InterferingSignal Transductionbcl-2-Associated X ProteinGW 311616Leukocyte ElastasePhosphatidylinositol 3-KinasesPiperidinesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2RNA, Small Interfering

Identifiers

PMID26081156
PMCPMC4526057
OpenAlexW2109423564

What OpenQuestion holds

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Registered trials

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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.