Evidence map›Paper›PMID 27992365›Full record

ArticleOncotarget2017

Gankyrin promotes epithelial-mesenchymal transition and metastasis in NSCLC through forming a closed circle with IL-6/ STAT3 and TGF-β/SMAD3 signaling pathway.

Wu-Ping Wang, Ying Sun, Qiang Lu, Jin-Bo Zhao, Xue-Jiao Wang, Zhao Chen, Yun-Feng Ni, Ju-Zheng Wang, Yong Han, Zhi-Pei Zhang and 2 more

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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 27 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

12 authors at 1 institution in 1 country.

Wu-Ping WangDepartment of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, China.
Ying SunDepartment of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, China.
Qiang LuDepartment of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, China.
Jin-Bo ZhaoDepartment of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, China.
Xue-Jiao WangDepartment of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, China.
Zhao ChenDepartment of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, China.
Yun-Feng NiDepartment of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, China.
Ju-Zheng WangDepartment of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, China.
Yong HanDepartment of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, China.
Zhi-Pei ZhangDepartment of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, China.
Xiao-Long YanDepartment of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, China.
Xiao-Fei LiDepartment of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University, Xi'an, 710038, China.
Air Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous research showed that Gankyrin was overexpressed in NSCLC and significantly associated with clinicopathologic features and poor prognosis. In this study, we will explore potential effect of Gankyrin on EMT and metastasis in NSCLC. The ectopic higher expression of Gankyrin markedly increased the migration and invasion in NSCLC cells. In contrast, silencing Gankyrin inhibit this aggressive behavior in NSCLC cells. Further study demonstrated that overexpression of Gankyrin could decrease E-cadherin expression and increase expression of Vimentin and Twist1 at mRNA and protein levels. These data indicated that Gankyrin could facilitate occurrence and development of EMT. Also IHC analysis showed that Gankyrin expression was negatively correlated with E-cadherin expression, while positively correlated with Vimentin and Twist1 expression in NSCLC tissues. The mechanism study finally suggested that the Gankyrin-driven EMT was partially due to IL-6/p-STAT3 and TGF-β/p-SMAD3 pathways activation. Taken together, our data provided a novel mechanism of Gankyrin promoting EMT and metastasis in NSCLC through forming a closed circle with IL-6/p-STAT3 and TGF-β/p-SMAD3 signaling pathway.

Indexed as

A549 CellsCarcinoma, Non-Small-Cell LungCell Line, TumorEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansInterleukin-6Lung NeoplasmsNeoplasm MetastasisProteasome Endopeptidase ComplexProto-Oncogene ProteinsSignal TransductionSmad3 ProteinSTAT3 Transcription FactorTransforming Growth Factor betaUp-RegulationIL6 protein, humanInterleukin-6Proteasome Endopeptidase ComplexProto-Oncogene ProteinsPSMD10 protein, humanSmad3 ProteinSMAD3 protein, humanSTAT3 protein, humanSTAT3 Transcription FactorTransforming Growth Factor betaclosed circleEMTgankyrinmetastasisNSCLC

Identifiers

PMID27992365
PMCPMC5351600
OpenAlexW2564119591

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.