Evidence map›Paper›PMID 34738187›Full record

ArticleJournal of gastrointestinal cancer2021

Evaluation of ATAD2 as a Potential Target in Hepatocellular Carcinoma.

Umut Ekin, Haluk Yuzugullu, Cigdem Ozen, Peyda Korhan, Ezgi Bagirsakci, Funda Yilmaz, Ozge Gursoy Yuzugullu, Hamdiye Uzuner, Hani Alotaibi, Petek Ballar Kirmizibayrak and 3 more

Open access · bronzeAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in Journal of gastrointestinal cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.2field-weighted citation impact, top 50% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
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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 3 countries.

Umut EkinIzmir Biomedicine and Genome Center, Izmir, Turkey.
Haluk YuzugulluDepartment of Molecular Biology and Genetics, Bilkent University, Ankara, Turkey.
Cigdem OzenIzmir Biomedicine and Genome Center, Izmir, Turkey.
Peyda KorhanIzmir Biomedicine and Genome Center, Izmir, Turkey.
Ezgi BagirsakciIzmir Biomedicine and Genome Center, Izmir, Turkey.
Funda YilmazDepartment of Pathology, Faculty of Medicine, Ege University, Izmir, Turkey.
Ozge Gursoy YuzugulluDepartment of Molecular Biology and Genetics, Bilkent University, Ankara, Turkey.
Hamdiye UzunerIzmir Biomedicine and Genome Center, Izmir, Turkey.
Hani AlotaibiIzmir Biomedicine and Genome Center, Izmir, Turkey.
Petek Ballar KirmizibayrakDepartment of Biochemistry, Faculty of Pharmacy, Ege University, Izmir, Turkey.
Nese AtabeyIzmir Biomedicine and Genome Center, Izmir, Turkey.
Gökhan KarakülahIzmir Biomedicine and Genome Center, Izmir, Turkey.
Mehmet OzturkIzmir Biomedicine and Genome Center, Izmir, Turkey. mehmet.ozturk@ibg.edu.tr.ORCID http://orcid.org/0000-0002-6092-9706
Izmir University · TRBilkent University · TREge University · TR

Funding

Türkiye Bilimsel ve Teknolojik Araştirma Kurumu 109S191Türkiye Bilimsel ve Teknolojik Araştirma Kurumu 111T558
6 · The paper itself

Abstract

purposeHepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death worldwide with lack of effective systemic chemotherapy. In this study, we aimed to evaluate the value of ATPase family AAA domain-containing protein 2 (ATAD2) as a biomarker and potential therapeutic target for HCC.

methodsThe expression of ATAD2 was tested in different HCC patient cohorts by immunohistochemistry and comparative transcriptional analysis. The co-expression of ATAD2 and proliferation markers was compared during liver regeneration and malignancy with different bioinformatics tools. The cellular effects of ATAD2 inactivation in liver malignancy was tested on cell cycle, apoptosis, and colony formation ability as well as tumor formation using RNA interference. The genes affected by ATAD2 inactivation in three different HCC cell lines were identified by global gene expression profiling and bioinformatics tools.

resultsATAD2 overexpression is closely correlated with HCC tumor stage. There was gradual increase from dysplasia, well-differentiated and poorly-differentiated HCC, respectively. We also observed transient upregulation of ATAD2 expression during rat liver regeneration in parallel to changes in Ki-67 expression. ATAD2 knockdown resulted in apoptosis and decreased cell survival in vitro and decreased tumor formation in some HCC cell lines. However, three other HCC cell lines tested were not affected. Similarly, gene expression response to ATAD2 inactivation in different HCC cell lines was highly heterogeneous.

conclusionsATAD2 is a potential proliferation marker for liver regeneration and HCC. It may also serve as a therapeutic target despite heterogeneous response of malignant cells.

Indexed as

AnimalsApoptosisATPases Associated with Diverse Cellular ActivitiesBiomarkers, TumorCarcinoma, HepatocellularCell Line, TumorDNA-Binding ProteinsGene Expression Regulation, NeoplasticHumansKi-67 AntigenLiver NeoplasmsRatsATAD2 protein, humanATPases Associated with Diverse Cellular ActivitiesBiomarkers, TumorDNA-Binding ProteinsKi-67 AntigenApoptosisATAD2Gene expression profilesGene knock downLiver cancerProliferation

Identifiers

PMID34738187
OpenAlexW3200421305

What OpenQuestion holds

Textmetadata
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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.