Evidence map›Paper›PMID 28108731›Full record

ArticleOncotarget2017

Loss of endothelial cell-specific molecule 1 promotes the tumorigenicity and metastasis of prostate cancer cells through regulation of the TIMP-1/MMP-9 expression.

Chien-Min Chen, Chu-Liang Lin, Hui-Ling Chiou, Shu-Ching Hsieh, Chia-Liang Lin, Chun-Wen Cheng, Chia-Hung Hung, Jen-Pi Tsai, Yi-Hsien Hsieh

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

13 citing papers in PubMed, 22 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

9 authors at 3 institutions in 1 country.

Chien-Min ChenDivision of Neurosurgery, Department of Surgery, Changhua Christian Hospital, Changhua, Taiwan.
Chu-Liang LinInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Hui-Ling ChiouSchool of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan.
Shu-Ching HsiehSchool of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan.
Chia-Liang LinInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Chun-Wen ChengInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Chia-Hung HungInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Jen-Pi TsaiSchool of Medicine, Tzu Chi University, Hualien, Taiwan.
Yi-Hsien HsiehInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Chung Shan Medical University · TWChanghua Christian Hospital · TWTzu Chi University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Endothelial cell specific molecule-1 (ESM1) protein has been involved in proliferation and metastatic progression in multiple tumors. However, there are no studies regarding the mechanism of ESM1 in prostate cancer. We found that ESM1 knockdown in prostate cancer cells resulted in increased cell proliferation and colony formation ability response evidenced by decreased expression of p21 and increased expression of cyclin D1 in prostate cancer cells. Moreover, we revealed that knockdown ESM1 also induced the epithelial-mesenchymal transition (EMT), motility and invasiveness in accordance with the upregulated the MMP-9 expression, while downregulated the TIMP-1 expression. Recombinant human (Rh) TIMP-1 significantly attenuated ESM1-mediated cell migration and invasion. Additionally, ESM1 knockdown increased in vivo tumorigenicity and metastasis of prostate cancer cells. These findings provide the first evidence that the imbalance of MMP-9/TIMP-1, is one of the regulation mechanisms by which ESM1 promotes tumorigenicity and metastasis of prostate cancer cells.

Indexed as

AnimalsBlotting, WesternCell Line, TumorEpithelial-Mesenchymal TransitionFluorescent Antibody TechniqueGene Expression Regulation, NeoplasticGene Knockdown TechniquesHeterograftsHumansMaleMatrix Metalloproteinase 9MiceMice, NudeNeoplasm InvasivenessNeoplasm ProteinsPolymerase Chain ReactionESM1 protein, humanMatrix Metalloproteinase 9MMP9 protein, humanNeoplasm ProteinsProteoglycansTIMP1 protein, humanTissue Inhibitor of Metalloproteinase-1endothelial cell specific molecule 1epithelial-mesenchymal transitionmetastasisprostate cancer cellstumorigenicity

Identifiers

PMID28108731
PMCPMC5355147
OpenAlexW2574230745

What OpenQuestion holds

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LicenceCC BY
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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.