Evidence map›Paper›PMID 24849319›Full record

ArticlePloS one2014

IQGAP3 promotes EGFR-ERK signaling and the growth and metastasis of lung cancer cells.

Ying Yang, Wei Zhao, Qing-Wen Xu, Xiao-Song Wang, Yu Zhang, Jun Zhang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

54 citing papers in PubMed, 85 citations in OpenAlex.

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  11. IQGAP3 Is an Important Mediator of Skin Inflammatory Diseases.International journal of molecular sciences · 2024
    Article
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  14. FOXD2 regulations IQGAP3 mediated CaThe Kaohsiung journal of medical sciences · 2023
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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

6 authors at 1 institution in 1 country.

Ying YangDepartment of Immunology, School of Basic Medical Sciences, Key Laboratory of Medical Immunology of Ministry of Public Health, Peking University Health Science Center, Beijing, P. R. China.
Wei ZhaoDepartment of Immunology, School of Basic Medical Sciences, Key Laboratory of Medical Immunology of Ministry of Public Health, Peking University Health Science Center, Beijing, P. R. China.
Qing-Wen XuDepartment of Immunology, School of Basic Medical Sciences, Key Laboratory of Medical Immunology of Ministry of Public Health, Peking University Health Science Center, Beijing, P. R. China.
Xiao-Song WangDepartment of Immunology, School of Basic Medical Sciences, Key Laboratory of Medical Immunology of Ministry of Public Health, Peking University Health Science Center, Beijing, P. R. China.
Yu ZhangDepartment of Immunology, School of Basic Medical Sciences, Key Laboratory of Medical Immunology of Ministry of Public Health, Peking University Health Science Center, Beijing, P. R. China.
Jun ZhangDepartment of Immunology, School of Basic Medical Sciences, Key Laboratory of Medical Immunology of Ministry of Public Health, Peking University Health Science Center, Beijing, P. R. China.
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proteins of the IQGAP family display complicated and often contradictory activities in tumorigenesis. IQGAP1 has well documented oncogenic potential and IQGAP2 has putative tumor-suppressive function. IQGAP3 is the latest addition to this family and its role in cancer development remains to be defined. Here we demonstrate IQGAP3 expression is markedly increased in lung cancer tissues at both mRNA and protein levels. Overexpression of IQGAP3 promoted tumor cell growth, and migration and invasion, whereas knockdown of IQGAP3 exhibited opposite effects. Moreover, suppression of IQGAP3 in a lung cancer cell line caused a reduction in the tumorigenicity of these cells in lung tissue after intravenous injection. Furthermore, we showed that IQGAP3 is able to interact with ERK1 and enhance its phosphorylation following treatment with EGF. These data suggest that IQGAP3 may contribute to the pathogenesis of lung cancer by modulating EGFR-ERK signaling.

Indexed as

Signal TransductionCarcinogenesisCell Line, TumorCell MovementCell ProliferationErbB ReceptorsExtracellular Signal-Regulated MAP KinasesGene Knockdown TechniquesGTPase-Activating ProteinsHumansLung NeoplasmsNeoplasm InvasivenessNeoplasm MetastasisPhosphorylationUp-RegulationErbB ReceptorsExtracellular Signal-Regulated MAP KinasesGTPase-Activating ProteinsIQGAP3 protein, human

Identifiers

PMID24849319
PMCPMC4029748
OpenAlexW2130812687

What OpenQuestion holds

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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.