Evidence map›Paper›PMID 26561205›Full record

ArticleOncotarget2016

MDA-9/Syntenin-Slug transcriptional complex promote epithelial-mesenchymal transition and invasion/metastasis in lung adenocarcinoma.

Lu-Kai Wang, Szu-Hua Pan, Yih-Leong Chang, Pei-Fang Hung, Shih-Han Kao, Wen-Lung Wang, Ching-Wen Lin, Shuenn-Chen Yang, Chen-Hsien Liang, Chen-Tu Wu and 3 more

Abstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

21 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  16. Lung Adenocarcinoma Syndecan-2 Potentiates Cell Invasiveness.American journal of respiratory cell and molecular biology · 2019
    Article
  17. A PDZ Protein MDA-9/Syntenin: As a Target for Cancer Therapy.Computational and structural biotechnology journal · 2019
    Review
  18. Article
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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

13 authors.

Lu-Kai WangDepartment of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Szu-Hua PanGraduate Institute of Medical Genomics and Proteomics, College of Medicine, National Taiwan University, Taipei, Taiwan.
Yih-Leong ChangDepartment of Pathology and Graduate Institute of Pathology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Pei-Fang HungDepartment of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.
Shih-Han KaoResearch Center for Tumor Medical Science, China Medical University, Taichung, Taiwan.
Wen-Lung WangDepartment of Otolaryngology, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
Ching-Wen LinInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Shuenn-Chen YangInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Chen-Hsien LiangDivision of Isotope application, Institute of Nuclear Energy Research, Taoyuan, Taiwan.
Chen-Tu WuDepartment of Pathology and Graduate Institute of Pathology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Tzu-Hung HsiaoDepartment of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan.
Tse-Ming HongInstitute of Basic Medical Sciences, National Cheng Kung University, Tainan, Taiwan.
Pan-Chyr YangDepartment of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melanoma differentiation-associated gene-9 (MDA-9)/Syntenin is a novel therapeutic target because it plays critical roles in cancer progression and exosome biogenesis. Here we show that Slug, a key epithelial-mesenchymal-transition (EMT) regulator, is a MDA-9/Syntenin downstream target. Mitogen EGF stimulation increases Slug expression and MDA-9/Syntenin nuclear translocation. MDA-9/Syntenin uses its PDZ1 domain to bind with Slug, and this interaction further leads to HDAC1 recruitment, up-regulation of Slug transcriptional repressor activity, enhanced Slug-mediated EMT, and promotion of cancer invasion and metastasis. The PDZ domains and nuclear localization of MDA-9/Syntenin are both required for promoting Slug-mediated cancer invasion. Clinically, patients with high MDA-9/Syntenin and high Slug expressions were associated with poor overall survival compared to those with low expression in lung adenocarcinomas. Our findings provide evidence that MDA-9/Syntenin acts as a pivotal adaptor of Slug and it transcriptionally enhances Slug-mediated EMT to promote cancer invasion and metastasis.

Indexed as

AdenocarcinomaAnimalsCell Line, TumorEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHEK293 CellsHumansImmunoblottingLung NeoplasmsMaleMCF-7 CellsMice, Inbred NODMice, SCIDMicroscopy, ConfocalNeoplasm InvasivenessSDCBP protein, humanSNAI1 protein, humanSnai2 protein, mouseSnail Family Transcription FactorsSynteninsTranscription FactorsEMTinvasionlung adenocarcinomaSlugSyntenin

Identifiers

PMID26561205
PMCPMC4808006

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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.