Evidence map›Paper›PMID 24756349›Full record

ArticleJournal of neuro-oncology2014

Exogenous endothelin-1 induces cell migration and matrix metalloproteinase expression in U251 human glioblastoma multiforme.

Wen-Tsong Hsieh, Wei-Lan Yeh, Ruo-Yuo Cheng, Chingju Lin, Cheng-Fang Tsai, Bor-Ren Huang, Caren Yu-Ju Wu, Hsiao-Yun Lin, Shiang-Suo Huang, Dah-Yuu Lu

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Article in Journal of neuro-oncology, 2014. 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
1.9field-weighted citation impact, top 15% 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, 23 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

10 authors at 6 institutions in 1 country.

Wen-Tsong HsiehDepartment of Pharmacology, School of Medicine, China Medical University, Taichung, Taiwan.
Wei-Lan YehDepartment of Cell and Tissue Engineering and Department of Medical Research, Changhua Christian Hospital, Changhua, Taiwan.
Ruo-Yuo ChengDepartment of Pharmacology, School of Medicine, China Medical University, Taichung, Taiwan.
Chingju LinDepartment of Physiology, School of Medicine, China Medical University, Taichung, Taiwan.
Cheng-Fang TsaiDepartment of Biotechnology, Asia University, Taichung, Taiwan.
Bor-Ren HuangDepartment of Neurosurgery, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung, Taiwan.
Caren Yu-Ju WuGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
Hsiao-Yun LinDepartment of Life Sciences, National Chung Hsing University, Taichung, Taiwan.
Shiang-Suo HuangDepartment of Pharmacology and Institute of Medicine, College of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Dah-Yuu LuGraduate Institute of Neural and Cognitive Sciences, China Medical University, No. 91 Hsueh-Shih Road, Taichung, Taiwan. dahyuu@mail.cmu.edu.tw.
China Medical University · TWAsia University · TWChanghua Christian Hospital · TWChung Shan Medical University · TWNational Chung Hsing University · TWTaipei Tzu Chi Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is the most common and lethal type of primary brain tumor characterized by its rapid infiltration to surrounding tissues during the early stages. The fast spreading of GBM obscures the initiation of the tumor mass making the treatment outcome undesirable. Endothelin-1 is known as a secretory protein presented in various types of brain cells, which has been indicated as a factor for cancer pathology. The aim of the present study was to investigate the molecular mechanism of cell migration in GBM. We found that various malignant glioma cells expressed higher amounts of endothelin-1, ETA, and ETB receptors than nonmalignant human astrocytes. The application of endothelin-1 enhanced the migratory activity in human U251 glioma cells corresponding to increased expression of matrix metalloproteinase (MMP)-9 and MMP-13. The endothelin-1-induced cell migration was attenuated by MMP-9 and MMP-13 inhibitors and inhibitors of mitogen-activated protein (MAP) kinase and PI3 kinase/Akt. Furthermore, the elevated levels of phosphate c-Jun accumulation in the nucleus and activator protein-1 (AP-1)-DNA binding activity were also found in endothelin-1 treated glioma cells. In migration-prone sublines, cells with greater migration ability showed higher endothelin-1, ETB receptor, and MMP expressions. These results indicate that endothelin-1 activates MAP kinase and AP-1 signaling, resulting in enhanced MMP-9 and MMP-13 expressions and cell migration in GBM.

Indexed as

AstrocytesCell Line, TumorCell MovementCell NucleusCentral Nervous System NeoplasmsEndothelin-1Extracellular Signal-Regulated MAP KinasesGlioblastomaHumansJNK Mitogen-Activated Protein KinasesMatrix Metalloproteinase 13Matrix Metalloproteinase 9Phosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktReceptor, Endothelin AEndothelin-1Extracellular Signal-Regulated MAP KinasesJNK Mitogen-Activated Protein KinasesMatrix Metalloproteinase 13Matrix Metalloproteinase 9MMP13 protein, humanMMP9 protein, humanPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktReceptor, Endothelin AReceptor, Endothelin BTranscription Factor AP-1

Identifiers

PMID24756349
OpenAlexW1976446556

What OpenQuestion holds

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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.