Evidence map›Paper›PMID 26523208›Full record

ArticleJournal of cancer science & therapy2014

Combination Treatment with Apricoxib and IL-27 Enhances Inhibition of Epithelial-Mesenchymal Transition in Human Lung Cancer Cells through a STAT1 Dominant Pathway.

Mi-Heon Lee, Puja Kachroo, Paul C Pagano, Jane Yanagawa, Gerald Wang, Tonya C Walser, Kostyantyn Krysan, Sherven Sharma, Maie St John, Steven M Dubinett and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cancer science & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. 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

11 authors at 1 institution in 1 country.

Mi-Heon LeeLung Cancer Research Program, Jonsson Comprehensive Cancer Center, USA ; Division of Thoracic Surgery at the David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Puja KachrooLung Cancer Research Program, Jonsson Comprehensive Cancer Center, USA ; Division of Pulmonary and Critical Care Medicine, USA ; Division of Thoracic Surgery at the David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Paul C PaganoMolecular and Medical Pharmacology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Jane YanagawaLung Cancer Research Program, Jonsson Comprehensive Cancer Center, USA ; Division of Thoracic Surgery at the David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Gerald WangLung Cancer Research Program, Jonsson Comprehensive Cancer Center, USA ; Division of Pulmonary and Critical Care Medicine, USA.
Tonya C WalserLung Cancer Research Program, Jonsson Comprehensive Cancer Center, USA ; Division of Pulmonary and Critical Care Medicine, USA.
Kostyantyn KrysanLung Cancer Research Program, Jonsson Comprehensive Cancer Center, USA ; Division of Pulmonary and Critical Care Medicine, USA.
Sherven SharmaLung Cancer Research Program, Jonsson Comprehensive Cancer Center, USA ; Department of Head and Neck Surgery, David Geffen School of Medicine, University of California, Los Angeles, CA, USA ; Molecular Gene Medicine Laboratory, Veterans Affair Greater Los Angeles Healthcare System, Los Angeles, CA, USA.
Maie St JohnLung Cancer Research Program, Jonsson Comprehensive Cancer Center, USA ; Department of Head and Neck Surgery, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Steven M DubinettLung Cancer Research Program, Jonsson Comprehensive Cancer Center, USA ; Division of Pulmonary and Critical Care Medicine, USA ; Molecular Gene Medicine Laboratory, Veterans Affair Greater Los Angeles Healthcare System, Los Angeles, CA, USA.
Jay M LeeLung Cancer Research Program, Jonsson Comprehensive Cancer Center, USA ; Division of Pulmonary and Critical Care Medicine, USA ; Division of Thoracic Surgery at the David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
University of California, Los Angeles · US

Funding

UCLA Clinical and Translational Science InstituteUL1TR000124 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2012 to 2015
$57.0M
UCLA Pulmonary and Critical Care Medicine Training ProgramT32HL072752 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI JOHN A BELPERIO, TOMAS GANZ · 2003 to 2026
$8.3M
Gene Modified Dendritic Cell Therapy in Lung CancerK23CA131577 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LEE, JAY M · 2009 to 2013
$660k
NCATS NIH HHS UL1 TR000124NCI NIH HHS K23 CA131577NCI NIH HHS L30 CA142223NHLBI NIH HHS T32 HL072752
6 · The paper itself

Abstract

backgroundThe cyclooxygenase 2 (COX-2) pathway has been implicated in the molecular pathogenesis of many malignancies, including lung cancer. Apricoxib, a selective COX-2 inhibitor, has been described to inhibit epithelial-mesenchymal transition (EMT) in human malignancies. The mechanism by which apricoxib may alter the tumor microenvironment by affecting EMT through other important signaling pathways is poorly defined. IL-27 has been shown to have anti-tumor activity and our recent study showed that IL-27 inhibited EMT through a STAT1 dominant pathway.

objectiveThe purpose of this study is to investigate the role of apricoxib combined with IL-27 in inhibiting lung carcinogenesis by modulation of EMT through STAT signaling. METHODS AND

resultsWestern blot analysis revealed that IL-27 stimulation of human non-small cell lung cancer (NSCLC) cell lines results in STAT1 and STAT3 activation, decreased Snail protein and mesenchymal markers (N-cadherin and vimentin) and a concomitant increase in expression of epithelial markers (E-cadherin, β-and γ-catenins), and inhibition of cell migration. The combination of apricoxib and IL-27 resulted in augmentation of STAT1 activation. However, IL-27 mediated STAT3 activation was decreased by the addition of apricoxib. STAT1 siRNA was used to determine the involvement of STAT1 pathway in the enhanced inhibition of EMT and cell migration by the combined IL-27 and apricoxib treatment. Pretreatment of cells with STAT1 siRNA inhibited the effect of combined IL-27 and apricoxib in the activation of STAT1 and STAT3. In addition, the augmented expression of epithelial markers, decreased expression mesenchymal markers, and inhibited cell migration by the combination treatment were also inhibited by STAT1 siRNA, suggesting that the STAT1 pathway is important in the enhanced effect from the combination treatment.

conclusionCombined apricoxib and IL-27 has an enhanced effect in inhibition of epithelial-mesenchymal transition and cell migration in human lung cancer cells through a STAT1 dominant pathway.

Indexed as

A549ApricoxibCOX-2Epithelial-Mesenchymal TransitionIL-27Non-small cell lung cancerSTAT1STAT3

Identifiers

PMID26523208
PMCPMC4624255
OpenAlexW2002821216

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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.