Evidence map›Paper›PMID 26338423›Full record

ArticleScientific reports2015

EGFR-L858R mutant enhances lung adenocarcinoma cell invasive ability and promotes malignant pleural effusion formation through activation of the CXCL12-CXCR4 pathway.

Meng-Feng Tsai, Tzu-Hua Chang, Shang-Gin Wu, Hsiao-Yin Yang, Yi-Chiung Hsu, Pan-Chyr Yang, Jin-Yuan Shih

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 2 pooled it
4.5field-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

48 citing papers in PubMed, 2 syntheses or guidelines pooled it, 68 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

7 authors at 4 institutions in 1 country.

Meng-Feng TsaiDepartment of Molecular Biotechnology, College of Biotechnology and Bioresources, Dayeh University, Changhua 51591, Taiwan.
Tzu-Hua ChangDepartment of Internal Medicine, National Taiwan University Hospital, and College of Medicine, National Taiwan University, Taipei 10002, Taiwan.
Shang-Gin WuDepartment of Internal Medicine, National Taiwan University Hospital, Yun-Lin Branch, Yunlin 64041, Taiwan.
Hsiao-Yin YangDepartment of Internal Medicine, National Taiwan University Hospital, and College of Medicine, National Taiwan University, Taipei 10002, Taiwan.
Yi-Chiung HsuInstitute of Statistical Science, Academia Sinica, Taipei 11529, Taiwan.
Pan-Chyr YangDepartment of Internal Medicine, National Taiwan University Hospital, and College of Medicine, National Taiwan University, Taipei 10002, Taiwan.
Jin-Yuan ShihDepartment of Internal Medicine, National Taiwan University Hospital, and College of Medicine, National Taiwan University, Taipei 10002, Taiwan.
National Taiwan University Hospital · TWNational Taiwan University · TWDayeh University · TWInstitute of Statistical Science, Academia Sinica · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant pleural effusion (MPE) is a common clinical problem in non-small cell lung carcinoma (NSCLC) patients; however, the underlying mechanisms are still largely unknown. Recent studies indicate that the frequency of the L858R mutant form of the epidermal growth factor receptor (EGFR-L858R) is higher in lung adenocarcinoma with MPE than in surgically resected specimens, suggesting that lung adenocarcinoma cells harboring this mutation tend to invade the adjacent pleural cavity. The purpose of this study was to clarify the relationship between the EGFR-L858R mutation and cancer cell invasion ability and to investigate the molecular mechanisms involved in the formation of MPE. We found that expression of EGFR-L858R in lung cancer cells resulted in up-regulation of the CXCR4 in association with increased cancer cell invasive ability and MPE formation. Ectopic expression of EGFR-L858R in lung cancer cells acted through activation of ERK signaling pathways to induce the expression of CXCR4. We also indicated that Inhibition of CXCR4 with small interfering RNA, neutralizing antibody, or receptor antagonist significantly suppressed the EGFR-L858R-dependent cell invasion. These results suggest that targeting the production of CXCR4 and blocking the CXCL12-CXCR4 pathway might be effective strategies for treating NSCLCs harboring a specific type of EGFR mutation.

Indexed as

AdenocarcinomaCell Line, TumorChemokine CXCL12ErbB ReceptorsHumansLung NeoplasmsMutationNeoplasm InvasivenessPleural Effusion, MalignantReceptors, CXCR4Signal TransductionChemokine CXCL12CXCL12 protein, humanCXCR4 protein, humanEGFR protein, humanErbB ReceptorsReceptors, CXCR4

Identifiers

PMID26338423
PMCPMC4559673
OpenAlexW2414722525

What OpenQuestion holds

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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.