Evidence map›Paper›PMID 29285847›Full record

ArticleCancer science2018

2-anilino-4-amino-5-aroylthiazole-type compound AS7128 inhibits lung cancer growth through decreased iASPP and p53 interaction.

Hao-Wei Cheng, Rong-Jie Chein, Ting-Jen Cheng, Pei-Shan Wu, Hsin-Yi Wu, Pei-Fang Hung, Chia-Jen Wang, Yuan-Ling Hsu, Jau-Min Wong, Ang Yuan and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 45% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
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 6 institutions in 1 country.

Hao-Wei ChengInstitute of Biomedical Engineering, National Taiwan University, Taipei, Taiwan.
Rong-Jie CheinInstitute of Chemistry, Academia Sinica, Taipei, Taiwan.
Ting-Jen ChengGenomics Research Center, Academia Sinica, Taipei, Taiwan.
Pei-Shan WuGenome and Systems Biology Degree Program, National Taiwan University and Academia Sinica, Taipei, Taiwan.
Hsin-Yi WuInstitute of Chemistry, Academia Sinica, Taipei, Taiwan.
Pei-Fang HungInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Chia-Jen WangInstitute of Stem Cell and Translational Cancer Research, Chang Gung Memorial Hospital, Taoyuan, Taiwan.
Yuan-Ling HsuGraduate Institute of Medical Genomics and Proteomics, National Taiwan University, Taipei, Taiwan.
Jau-Min WongInstitute of Biomedical Engineering, National Taiwan University, Taipei, Taiwan.
Ang YuanDepartment of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Chi-Huey WongGenomics Research Center, Academia Sinica, Taipei, Taiwan.
Pan-Chyr YangInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Szu-Hua PanGenome and Systems Biology Degree Program, National Taiwan University and Academia Sinica, Taipei, Taiwan.ORCID http://orcid.org/0000-0002-0138-0434
National Taiwan University · TWGenomics Research Center, Academia Sinica · TWInstitute of Biomedical Sciences, Academia Sinica · TWInstitute of Chemistry, Academia Sinica · TWChang Gung Memorial Hospital · TWNational Taiwan University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the leading cause of cancer-related death worldwide. Thus, developing novel therapeutic agents has become critical for lung cancer treatment. In this study, compound AS7128 was selected from a 2-million entry chemical library screening and identified as a candidate drug against non-small cell lung cancer in vitro and in vivo. Further investigation indicated that AS7128 could induce cell apoptosis and cell cycle arrest, especially in the mitosis stage. In addition, we also found that iASPP, an oncogenic protein that functionally inhibits p53, might be associated with AS7128 through mass identification. Further exploration indicated that AS7128 treatment could restore the transactivation ability of p53 and, thus, increase the expressions of its downstream target genes, which are related to cell cycle arrest and apoptosis. This occurs through disruption of the interactions between p53 and iASPP in cells. Taken together, AS7128 could bind to iASPP, disrupt the interaction between iASPP and p53, and result in cell cycle arrest and apoptosis. These findings may provide new insight for using iASPP as a therapeutic target for non-small cell lung cancer treatment.

Indexed as

A549 CellsAnimalsAntineoplastic AgentsCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsLung NeoplasmsMiceProtein BindingRepressor ProteinsThiazolesTumor Suppressor Protein p53Antineoplastic AgentsAS7128Intracellular Signaling Peptides and ProteinsPPP1R13L protein, humanRepressor ProteinsThiazolesTP53 protein, humanTumor Suppressor Protein p53apoptosiscell cycleiASPPlung cancerp53

Identifiers

PMID29285847
PMCPMC5834782
OpenAlexW2779602110

What OpenQuestion holds

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LicenceCC BY-NC
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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.