Evidence map›Paper›PMID 27694834›Full record

ArticleOncogenesis2016

DUOX1 silencing in lung cancer promotes EMT, cancer stem cell characteristics and invasive properties.

A C Little, D Sham, M Hristova, K Danyal, D E Heppner, R A Bauer, L M Sipsey, A Habibovic, A van der Vliet

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogenesis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 69 citations in OpenAlex.

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  13. Overexpression ofGland surgery · 2022
    Article
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  17. DUOX1 in mammalian disease pathophysiology.Journal of molecular medicine (Berlin, Germany) · 2021
    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

9 authors at 1 institution in 1 country.

A C LittleDepartment of Pathology and Laboratory Medicine, University of Vermont, Burlington, VT, USA.
D ShamDepartment of Pathology and Laboratory Medicine, University of Vermont, Burlington, VT, USA.
M HristovaDepartment of Pathology and Laboratory Medicine, University of Vermont, Burlington, VT, USA.
K DanyalDepartment of Pathology and Laboratory Medicine, University of Vermont, Burlington, VT, USA.
D E HeppnerDepartment of Pathology and Laboratory Medicine, University of Vermont, Burlington, VT, USA.
R A BauerDepartment of Pathology and Laboratory Medicine, University of Vermont, Burlington, VT, USA.
L M SipseyDepartment of Pathology and Laboratory Medicine, University of Vermont, Burlington, VT, USA.
A HabibovicDepartment of Pathology and Laboratory Medicine, University of Vermont, Burlington, VT, USA.
A van der VlietDepartment of Pathology and Laboratory Medicine, University of Vermont, Burlington, VT, USA.
University of Vermont · US

Funding

Multidisciplinary Training in Lung BiologyT32HL076122 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI IRVIN, CHARLES G, POYNTER, MATTHEW E · 2004 to 2023
$6.1M
Dual Oxidase in Airway Epithelial Repair and RemodelingR01HL085646 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI VAN DER VLIET, ALBERT · 2008 to 2020
$4.7M
Investigations of Redox-dependent Processes of the Airway EpitheliumF32HL129706 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI HEPPNER, DAVID E. · 2016 to 2016
$50k
NHLBI NIH HHS F32 HL129706NHLBI NIH HHS R01 HL085646NHLBI NIH HHS T32 HL076122
6 · The paper itself

Abstract

Dual oxidase 1 (DUOX1) is an oxidant-generating enzyme within the airway epithelium that participates in innate airway host defense and epithelial homeostasis. Recent studies indicate that DUOX1 is suppressed in lung cancers by epigenetic silencing, although the importance of DUOX1 silencing in lung cancer development or progression is unknown. Here we show that loss of DUOX1 expression in a panel of lung cancer cell lines is strongly associated with loss of the epithelial marker E-cadherin. Moreover, RNAi-mediated DUOX1 silencing in lung epithelial cells and the cancer cell line NCI-H292 was found to result in loss of epithelial characteristics/molecular features (altered morphology, reduced barrier function and loss of E-cadherin) and increased mesenchymal features (increased migration, anchorage-independent growth and gain of vimentin/collagen), suggesting a direct contribution of DUOX1 silencing to epithelial-to-mesenchymal transition (EMT), an important feature of metastatic cancer. Conversely, overexpression of DUOX1 in A549 cells was capable of reversing EMT features. DUOX1 silencing in H292 cells also led to enhanced resistance to epidermal growth factor receptor tyrosine kinase inhibitors such as erlotinib, and enhanced levels of cancer stem cell (CSC) markers CD133 and ALDH1. Furthermore, acquired resistance of H292 cells to erlotinib resulted in enhanced EMT and CSC features, as well as loss of DUOX1. Finally, compared with control H292 cells, H292-shDUOX1 cells displayed enhanced invasive features in vitro and in vivo. Collectively, our findings indicate that DUOX1 silencing in lung epithelial cancer cells promotes features of EMT, and may be strongly associated with invasive and metastatic lung cancer.

Identifiers

PMID27694834
PMCPMC5117847
OpenAlexW2528521470

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.