Evidence map›Paper›PMID 32015686›Full record

ArticleInternational journal of biological sciences2020

TFAP2A Induced ITPKA Serves as an Oncogene and Interacts with DBN1 in Lung Adenocarcinoma.

Zhou Guoren, Fan Zhaohui, Zhu Wei, Wang Mei, Wu Yuan, Shi Lin, Xu Xiaoyue, Zhang Xiaomei, Shen Bo

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 37 citations in OpenAlex.

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  9. Translational lung cancer research · 2024
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  12. Unraveling a Key Molecular Player Governing Pulmonary Alveolar Development.American journal of respiratory cell and molecular biology · 2024
    Article
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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 3 institutions in 1 country.

Zhou GuorenJiangsu Cancer Hospital, Jiangsu Institute Of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital; 42 Baiziting, Nanjing, Jiangsu, 210009, China (Corresponding Address).
Fan ZhaohuiJiangsu Cancer Hospital, Jiangsu Institute Of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital; 42 Baiziting, Nanjing, Jiangsu, 210009, China (Corresponding Address).
Zhu WeiSchool Of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.
Wang MeiSchool Of Medicine, Jiangsu University, Zhenjiang, Jiangsu, China.
Wu YuanJiangsu Cancer Hospital, Jiangsu Institute Of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital; 42 Baiziting, Nanjing, Jiangsu, 210009, China (Corresponding Address).
Shi LinJiangsu Cancer Hospital, Jiangsu Institute Of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital; 42 Baiziting, Nanjing, Jiangsu, 210009, China (Corresponding Address).
Xu XiaoyueJiangsu Cancer Hospital, Jiangsu Institute Of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital; 42 Baiziting, Nanjing, Jiangsu, 210009, China (Corresponding Address).
Zhang XiaomeiJiangsu Cancer Hospital, Jiangsu Institute Of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital; 42 Baiziting, Nanjing, Jiangsu, 210009, China (Corresponding Address).
Shen BoJiangsu Cancer Hospital, Jiangsu Institute Of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital; 42 Baiziting, Nanjing, Jiangsu, 210009, China (Corresponding Address).
Jiangsu Cancer Hospital · CNJiangsu University · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The inositol polyphosphate kinase (IPK) family member ITPKA (inositol 1,4,5-trisphosphate 3-kinase) regulates the levels of many inositol polyphosphates which are important in cellular signaling. Several recent studies reported the aberrant expression of ITPKA in malignancy disease and usually made cancer more aggressive. However, the contribution of the inositol polyphosphate kinase ITPKA to lung cancer development remains unclear. Here we report that ITPKA is overexpressed in lung adenocarcinoma (LUAD) and positively correlated with advanced clinical parameters. ITPKA contributes to the malignant phenotypes

Indexed as

Adenocarcinoma of LungBlotting, WesternCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionFlow CytometryGene Expression Regulation, NeoplasticHumansImmunohistochemistryImmunoprecipitationLung NeoplasmsNeuropeptidesPhosphotransferases (Alcohol Group Acceptor)Protein BindingTranscription Factor AP-2drebrinsInositol 1,4,5-trisphosphate 3-kinaseNeuropeptidesPhosphotransferases (Alcohol Group Acceptor)TFAP2A protein, humanTranscription Factor AP-2Drebrin 1EMTITPKALUADTFAP2A

Identifiers

PMID32015686
PMCPMC6990902
OpenAlexW2999130863

What Socratic holds

Textmetadata
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 Socratic graph.