Evidence map›Paper›PMID 26351076›Full record

ArticleJournal of translational medicine2015

STAT1 modification improves therapeutic effects of interferons on lung cancer cells.

Junjie Chen, Jialu Zhao, Lefu Chen, Nian Dong, Zhaojian Ying, Zhenzhen Cai, Dongxiang Ji, Yong Zhang, Li Dong, Yuping Li and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 39 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

13 authors at 3 institutions in 2 countries.

Junjie ChenDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. jiestory414@163.com.
Jialu ZhaoDepartment of Pulmonary Medicine, Lishui Central Hospital, The Fifth Affiliated Hospital of Wenzhou Medical University, Lishui Hospital of Zhejiang University, Lishui, Zhejiang, China. zhaojialu521@126.com.
Lefu ChenDepartment of Neurosurgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China. chenlefu915@163.com.
Nian DongDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. 154598090@qq.com.
Zhaojian YingDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. yingzj0577@126.com.
Zhenzhen CaiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. 670775624@qq.com.
Dongxiang JiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. 251354702@qq.com.
Yong ZhangDrug Discovery Program, Pulmonary and Critical Care Medicine, Department of Medicine, Washington University, St. Louis, MO, USA. yzhang@dom.wustl.edu.
Li DongDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. conniejs1984@163.com.
Yuping LiDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. wzliyp@163.com.
Lei JiangCentral Laboratory, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China. jiangleistone79@163.com.
Michael J HoltzmanDrug Discovery Program, Pulmonary and Critical Care Medicine, Department of Medicine, Washington University, St. Louis, MO, USA. holtzmanm@wustl.edu.
Chengshui ChenDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, Zhejiang, China. chenchengshui@126.com.
First Affiliated Hospital of Wenzhou Medical University · CNWenzhou Medical University · CNWashington University in St. Louis · US

Funding

Tissue and Cell Processing CoreU19AI070489 · NIAID · WASHINGTON UNIVERSITY · PI HOLTZMAN, MICHAEL J · 2006 to 2016
$17.9M
INTERFERON SIGNAL ENHANCERS AS ANTIVIRAL THERAPEUTICSR01AI111605 · NIAID · WASHINGTON UNIVERSITY · PI HOLTZMAN, MICHAEL J · 2014 to 2017
$1.8M
NIAID NIH HHS R01 AI111605NIAID NIH HHS U19 AI070489NIAID NIH HHS U19-AI070489
6 · The paper itself

Abstract

backgroundInterferons (IFNs) have potent anti-proliferative, pro-apoptotic, and immunomodulatory activities against cancer. However, the clinical utility of IFNs is limited by toxicity and pharmacokinetics making it difficult to achieve sustained therapeutic levels especially in solid tumors.

methodsSignal Transducer and Activator of Transcription 1 (STAT1) or a modified STAT1 (designated STAT1-CC) that is hyper-responsive to IFN were overexpressed in lung cancer SPC-A-1 and H1299 cells using lentiviral vectors. Transduction efficiency was monitored using enhanced green fluorescent protein (EGFP) expression. After transduction, cells were treated with interferon-gamma (IFN-γ) or interferon-beta (IFN-β) and monitored for cell proliferation, migration, and invasiveness using Cell Counting Kit-8 and transwell chamber assays and for apoptosis using Annexin V detection by flow cytometry. In addition, levels of STAT1, STAT1 Tyr-701 phosphorylation (pSTAT1), fibronectin, and β-catenin were determined using western blotting. In the case of IFN-γ stimulation, levels of S100A4, proliferating cell nuclear antigen (PCNA), and c-fos expression were also determined.

resultsWe found that expression of STAT1 or STAT1-CC enhanced the effect of IFN-γ and, IFN-β on inhibition of human lung cancer cell proliferation, migration and invasiveness. Moreover, STAT1 and STAT1-CC expression caused increases in pSTAT1 and decreases in fibronectin and β-catenin levels. STAT1-CC showed increased effects compared to STAT1 on IFN-γ induced pSTAT1 and down-regulation of S100A4, PCNA, and c-fos levels.

conclusionThe results show that STAT1-CC exhibited more strength in improving the antitumor response of IFNs in lung cancer cells. Results from this study suggest that combined treatment of IFNs and STAT1-CC might be a feasible approach for the clinical management of lung cancer in the future.

Indexed as

Gene Expression Regulation, NeoplasticAntineoplastic AgentsApoptosisbeta CateninCell Line, TumorCell MovementCell ProliferationCell SurvivalFibronectinsGreen Fluorescent ProteinsHEK293 CellsHumansInterferon-betaInterferon-gammaLung NeoplasmsNeoplasm InvasivenessAntineoplastic Agentsbeta CateninFibronectinsGreen Fluorescent ProteinsInterferon-betaInterferon-gammaSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID26351076
PMCPMC4562290
OpenAlexW2097137932

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.