Evidence map›Paper›PMID 27533453›Full record

ArticleOncotarget2016

Gli promotes epithelial-mesenchymal transition in human lung adenocarcinomas.

Hui Li, Dongsheng Yue, Joy Q Jin, Gavitt A Woodard, Bhairavi Tolani, Thomas M Luh, Etienne Giroux-Leprieur, Minli Mo, Zhao Chen, Juanjuan Che and 7 more

Open access · diamondAbstract 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 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. HHIP's dynamic role in epithelial wound healing reveals a potential mechanism of COPD susceptibility.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  9. NRF2 and Primary Cilia: An Emerging Partnership.Antioxidants (Basel, Switzerland) · 2020
    Review
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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

17 authors at 4 institutions in 2 countries.

Hui LiThoracic Oncology Program, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA 94115, USA.
Dongsheng YueThoracic Oncology Program, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA 94115, USA.
Joy Q JinThoracic Oncology Program, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA 94115, USA.
Gavitt A WoodardThoracic Oncology Program, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA 94115, USA.
Bhairavi TolaniThoracic Oncology Program, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA 94115, USA.
Thomas M LuhThoracic Oncology Program, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA 94115, USA.
Etienne Giroux-LeprieurThoracic Oncology Program, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA 94115, USA.
Minli MoBeijing ACCB Biotech Ltd., Beijing 100084, China.
Zhao ChenBeijing ACCB Biotech Ltd., Beijing 100084, China.
Juanjuan CheDepartment of Oncology, Beijing Friendship Hospital of Capital Medical University, Beijing 100050, China.
Zhenfa ZhangDepartment of Lung Cancer, Lung Cancer Center, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China.
Yong ZhouThoracic Oncology Program, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA 94115, USA.
Lei WangThoracic Oncology Program, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA 94115, USA.
Xishan HaoDepartment of Lung Cancer, Lung Cancer Center, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China.
David JablonsThoracic Oncology Program, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA 94115, USA.
Changli WangDepartment of Lung Cancer, Lung Cancer Center, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, China.
Biao HeThoracic Oncology Program, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA 94115, USA.
UCSF Helen Diller Family Comprehensive Cancer Center · USTianjin Medical University Cancer Institute and Hospital · CNUniversity of California, San Francisco · USCapital Medical 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 R01 CA125030
6 · The paper itself

Abstract

Adenocarcinoma is the most common type of lung cancer. Epithelial-mesenchymal transition (EMT) is required for tumor invasion/metastasis and the components that control this process are potential therapeutic targets. This study we examined the role of Gli in lung adenocarcinoma and whether its activation regulates metastasis through EMT in lung adenocarcinoma. We found that tumors with high Gli expression had significantly lower E-Cadherin expression in two independent cohorts of patients with lung adenocarcinoma that we studied. In vitro up-regulation of SHh resulted in increased cell migration while small molecule inhibitors of Smo or Gli significantly reduced cell mobility both in a wound healing assay and in a 3D cell invasion assay. Inhibition of Gli in vivo decreased tumor growth and induced an increase in E-Cadherin expression. Our results indicate that Gli may be critical for lung adenocarcinoma metastasis and that a novel Gli inhibitor shows promise as a therapeutic agent by preventing cell migration and invasion in vitro and significantly reducing tumor growth and increasing E-Cadherin expression in vivo.

Indexed as

Epithelial-Mesenchymal TransitionA549 CellsAdenocarcinomaAdenocarcinoma of LungAnimalsAntigens, CDAntineoplastic AgentsCadherinsCell MovementFemaleGene Expression Regulation, NeoplasticHedgehog ProteinsHumansLung NeoplasmsMaleMice, NudeAntigens, CDAntineoplastic AgentsCadherinsCDH1 protein, humanGLI1 protein, humanHedgehog ProteinsSHH protein, humanSmoothened ReceptorSMO protein, humanZinc Finger Protein GLI1adenocarcinomaepithelial-mesenchymal transitionglilung cancersonic hedgehog

Identifiers

PMID27533453
PMCPMC5348330
OpenAlexW2512251882

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.