Evidence map›Paper›PMID 29393489›Full record

ArticleMolecular medicine reports2018

Lysyl oxidase inhibition via β-aminoproprionitrile hampers human umbilical vein endothelial cell angiogenesis and migration in vitro.

Lin Shi, Ning Zhang, Hetao Liu, Lei Zhao, Jing Liu, Juan Wan, Wenyi Wu, Hetian Lei, Rongqing Liu, Mei Han

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  6. Lysyl Oxidase Family Enzymes and Their Role in Tumor Progression.International journal of molecular sciences · 2022
    Review
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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

10 authors at 3 institutions in 2 countries.

Lin ShiDepartment of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Ning ZhangDepartment of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Hetao LiuDepartment of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Lei ZhaoDepartment of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Jing LiuDepartment of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Juan WanDepartment of Rheumatology and Immunology, The General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Wenyi WuSchepens Eye Research Institute of Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA.
Hetian LeiSchepens Eye Research Institute of Massachusetts Eye and Ear, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA.
Rongqing LiuDepartment of Rheumatology and Immunology, The General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Mei HanDepartment of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, Ningxia 750004, P.R. China.
Ningxia Medical University · CNHarvard University · USSmith-Kettlewell Eye Research Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lysyl oxidase (LOX) is an enzyme that oxidizes lysine residues in collagens and elastin. It stabilizes or remodels the extracellular matrix and basement membrane of blood vessels. Current oncology studies have revealed that LOX is upregulated in invasive cancer cells and bolstered cell movement, and LOX was observed to promote the angiogenesis and migration of endothelial cells. In the present study, angiogenesis and migration were examined in human umbilical vein endothelial cells (HUVECs). Following cell treatment with 0.1-0.4 mM β-aminoproprionitrile (BAPN), a specific inhibitor of LOX, angiogenesis was analyzed with a fibrin gel in vitro angiogenesis assay kit and migration was examined via a Boyden Chamber assay. Angiogenesis-associated gene expression was investigated with a microarray assay and confirmed with reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The results showed that HUVEC angiogenesis substantially increased in the presence of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and phorbol 12-myristate 13-acetate (PMA). In addition, LOX inhibition blocked the angiogenesis stimulated by VEGF bFGF and PMA, and the inhibition of LOX reduced the migration of HUVECs. Furthermore, the microarray and RT-qPCR revealed that BAPN downregulated myeloid progenitor inhibitory factor 1, and western blot analysis demonstrated that BAPN decreased the phosphorylation of MAPK and Akt, suggesting that the specific inhibitor of LOX, BAPN, may serve as an alternative strategy for preventing angiogenesis.

Indexed as

AminopropionitrileBiomarkersCell MovementChemokines, CCFibroblast Growth FactorsGene Expression RegulationHumansHuman Umbilical Vein Endothelial CellsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Neovascularization, PhysiologicPhosphorylationProtein-Lysine 6-OxidaseProto-Oncogene Proteins c-aktVascular Endothelial Growth FactorsAminopropionitrileBiomarkersCCL23 protein, humanChemokines, CCFibroblast Growth FactorsMAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Protein-Lysine 6-OxidaseProto-Oncogene Proteins c-aktVascular Endothelial Growth Factorsangiogenesishuman umbilical vein endothelial celllysyl oxidasemigrationmyeloid progenitor inhibitory factor 1phospho-mitogen-activated protein kinasephospho-protein kinase B

Identifiers

PMID29393489
PMCPMC5865964
OpenAlexW2788242119

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.