Evidence map›Paper›PMID 24758269›Full record

ArticleJournal of experimental & clinical cancer research : CR2014

Hedgehog/Gli promotes epithelial-mesenchymal transition in lung squamous cell carcinomas.

Dongsheng Yue, Hui Li, Juanjuan Che, Yi Zhang, Hsin-Hui K Tseng, Joy Q Jin, Thomas M Luh, Etienne Giroux-Leprieur, Minli Mo, Qingfeng Zheng and 6 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
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  3. Translational lung cancer research · 2025
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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

16 authors at 7 institutions in 3 countries.

Dongsheng Yue
Hui Li
Juanjuan Che
Yi Zhang
Hsin-Hui K Tseng
Joy Q Jin
Thomas M Luh
Etienne Giroux-Leprieur
Minli Mo
Qingfeng Zheng
Huaiyin Shi
Hua Zhang
Xishan HaoDepartment of Lung Cancer, Lung Cancer Center, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China. yuedongsheng_cg@163.com.
Changli Wang
David M Jablons
Biao He
University of California, San Francisco · USTianjin Medical University Cancer Institute and Hospital · CNUCSF Helen Diller Family Comprehensive Cancer Center · USCapital Medical University · CNChinese PLA General Hospital · CNMinistry of Education · ETTsinghua University · CN

Funding

Small molecule inhibitors of Wnt-2 transcription in NSCLCR01CA125030 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HE, BIAO · 2009 to 2011
$952k
NCI NIH HHS R01CA125030
6 · The paper itself

Abstract

backgroundSquamous cell carcinomas (SCC) account for approximately 30% of non-small cell lung cancer. Investigation of the mechanism of invasion and metastasis of lung SCC will be of great help for the development of meaningful targeted therapeutics. This study is intended to understand whether the activation of Hedgehog (Hh) pathway is involved in lung SCC, and whether activated Hh signaling regulates metastasis through epithelial-mesenchymal transition (EMT) in lung SCC.

methodsTwo cohorts of patients with lung SCC were studied. Protein expression was examined by immunohistochemistry, Western blot, or immunofluorescence. Protein expression levels in tissue specimens were scored and correlations were analyzed. Vismodegib and a Gli inhibitor were used to inhibit Shh/Gli activity, and recombinant Shh proteins were used to stimulate the Hh pathway in lung SCC cell lines. Cell migration assay was performed in vitro.

resultsShh/Gli pathway components were aberrantly expressed in lung SCC tissue samples. Gli1 expression was reversely associated with the expression of EMT markers E-Cadherin and β-Catenin in lung SCC specimens. Inhibition of the Shh/Gli pathway suppressed migration and up-regulated E-Cadherin expression in lung SCC cells. Stimulation of the pathway increased migration and down-regulated E-Cadherin expression in lung SCC cells.

conclusionsOur results suggested that the Shh/Gli pathway may be critical for lung SCC recurrence, metastasis and resistance to chemotherapy. Inhibition of the Shh/Gli pathway activity/function is a potential therapeutic strategy for the treatment of lung SCC patients.

Indexed as

Epithelial-Mesenchymal TransitionAntigens, CDCadherinsCarcinoma, Squamous CellCell Line, TumorCell MovementDown-RegulationFemaleGene Expression Regulation, NeoplasticHedgehog ProteinsHumansLung NeoplasmsMaleMiddle AgedSignal TransductionTranscription FactorsAntigens, CDCadherinsCDH1 protein, humanGLI1 protein, humanHedgehog ProteinsTranscription FactorsZinc Finger Protein GLI1

Identifiers

PMID24758269
PMCPMC4029998
OpenAlexW2146731379

What OpenQuestion holds

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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.