Evidence map›Paper›PMID 26506240›Full record

ArticleOncotarget2015

Growth-arrest-specific 7C protein inhibits tumor metastasis via the N-WASP/FAK/F-actin and hnRNP U/β-TrCP/β-catenin pathways in lung cancer.

Ruo-Chia Tseng, Jer-Wei Chang, Jiou-Shan Mao, Charng-Dar Tsai, Pei-Chen Wu, Cuei-Jyuan Lin, Yi-Lin Lu, Sheng-You Liao, Hung-Chi Cheng, Han-Shui Hsu and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. 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
0.9field-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, 22 citations in OpenAlex.

  1. Article
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  3. Identification of Tumor Suppressive Genes Regulated byInternational journal of molecular sciences · 2021
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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

11 authors at 5 institutions in 1 country.

Ruo-Chia TsengDepartment of Molecular Biology and Human Genetics, College of Life Science, Tzu Chi University, Hualien, Taiwan.
Jer-Wei ChangInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan.
Jiou-Shan MaoDepartment of Pharmacology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Charng-Dar TsaiDepartment of Molecular Biology and Human Genetics, College of Life Science, Tzu Chi University, Hualien, Taiwan.
Pei-Chen WuDepartment of Molecular Biology and Human Genetics, College of Life Science, Tzu Chi University, Hualien, Taiwan.
Cuei-Jyuan LinInstitute of Medical Sciences, Tzu Chi University, Hualien, Taiwan.
Yi-Lin LuDepartment of Life Sciences, National Taiwan Normal University, Taipei, Taiwan.
Sheng-You LiaoInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Hung-Chi ChengDepartment of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Han-Shui HsuDivision of Thoracic Surgery, Taipei Veterans General Hospital, Institute of Emergency and Critical Care Medicine, National Yang-Ming University School of Medicine, Taipei, Taiwan.
Yi-Ching WangInstitute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan, Taiwan.
Tzu Chi University · TWNational Cheng Kung University · TWNational Health Research Institutes · TWNational Taiwan Normal University · TWTaipei Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growth-arrest-specific 7 (GAS7) belongs to a group of adaptor proteins that coordinate the actin cytoskeleton. Among human GAS7 isoforms, only GAS7C possesses a Src homology 3 domain. We report here that GAS7C acts as a migration suppressor and can serve as a prognostic biomarker in lung cancer. GAS7C overexpression reduces lung cancer migration, whereas GAS7C knockdown enhances cancer cell migration. Importantly, ectopically overexpressed GAS7C binds tightly with N-WASP thus inactivates the fibronectin/integrin/FAK pathway, which in turn leads to the suppression of F-actin dynamics. In addition, overexpression of GAS7C sequesters hnRNP U and thus decreases the level of β-catenin protein via the β-TrCP ubiquitin-degradation pathway. The anti-metastatic effect of GAS7C overexpression was also confirmed using lung cancer xenografts. Our clinical data indicated that 23.6% (25/106) of lung cancer patients showed low expression of GAS7C mRNA which correlated with a poorer overall survival. In addition, low GAS7C mRNA expression was detected in 60.0% of metastatic lung cancer patients, indicating an association between low GAS7C expression and cancer progression. A significant inverse correlation between mRNA expression and promoter hypermethylation was also found, which suggests that the low level of GAS7C expression was partly due to promoter hypermethylation. Our results provide novel evidence that low GAS7C correlates with poor prognosis and promotes metastasis in lung cancer. Low GAS7C increases cancer cell motility by promoting N-WASP/FAK/F-actin cytoskeleton dynamics. It also enhances β-catenin stability via hnRNP U/β-TrCP complex formation. Therefore, GAS7C acts as a metastasis suppressor in lung cancer.

Indexed as

Cell MovementActinsAnimalsBase Sequencebeta Cateninbeta-Transducin Repeat-Containing ProteinsCell Line, TumorCytoskeletonDNA MethylationFemaleFocal Adhesion Kinase 1Gene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHeterogeneous-Nuclear RibonucleoproteinsHumansLung NeoplasmsActinsbeta Cateninbeta-Transducin Repeat-Containing ProteinsBTRC protein, humanCTNNB1 protein, humanFocal Adhesion Kinase 1GAS7 protein, humanHeterogeneous-Nuclear RibonucleoproteinsNerve Tissue ProteinsPTK2 protein, humanWASL protein, humanWiskott-Aldrich Syndrome Protein, NeuronalGAS7ChnRNP Ulung cancerN-WASPprognosis

Identifiers

PMID26506240
PMCPMC4792552
OpenAlexW1838207691

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.