Evidence map›Paper›PMID 23954442›Full record

ArticleBiochimica et biophysica acta2013

Epigenetic upregulation of Bak by ZBP-89 inhibits the growth of hepatocellular carcinoma.

Cai Guo Ye, George G Chen, Rocky L K Ho, Juanita L Merchant, Ming-Liang He, Paul B S Lai

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

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  9. The anticancer effects of Resina Draconis extract on cholangiocarcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  10. Article
  11. Recognition Code of ZNF191(243-368) and Its Interaction with DNA.Bioinorganic chemistry and applications · 2015
    Article
  12. 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

6 authors at 3 institutions in 3 countries.

Cai Guo YeDepartment of Surgery, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong; China-America Cancer Research Institute, Guangdong Medical College, Dongguan 523808, PR China.
George G ChenDepartment of Surgery, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong. Electronic address: gchen@cuhk.edu.hk.
Rocky L K HoDepartment of Surgery, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong.
Juanita L MerchantInternal Medicine-Gastroenterology, University of Michigan, Ann Arbor, MI 48109, USA; Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA.
Ming-Liang HeStanley Ho Centre for Emerging Infectious Diseases, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong; School of Public Health and Primary Care, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong.
Paul B S LaiDepartment of Surgery, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong.
Chinese University of Hong Kong · HKGuangdong Medical College · CNUniversity of Michigan · US

Funding

Mechanisms of Gastrointestional Growth &TransformationR01DK055732 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MERCHANT, JUANITA L. · 2000 to 2014
$4.1M
NIDDK NIH HHS R01 DK055732
6 · The paper itself

Abstract

Zinc-binding protein-89 regulates Bak to facilitate apoptosis in cancer cells. This study examined if zinc-binding protein-89 regulates Bak through an epigenetic mechanism in hepatocellular carcinoma. We first demonstrated that the expression of Bak was reduced but the levels of deoxyribonucleic acid methyltransferase 1 and histone deacetylase 3 were increased in hepatocellular carcinoma cancer tissues compared to the corresponding non-cancer tissues. Moreover, there was a negative correlation between Bak expression and deoxyribonucleic acid methyltransferase 1 levels in hepatocellular carcinoma. Administration of zinc-binding protein-89 downregulated histone deacetylase 3 expression and suppressed the activities of histone deacetylase and deoxyribonucleic acid methyltransferase, which led to maintenance of histone acetylation status, inhibited the binding of methyl-CpG-binding protein 2 to genomic deoxyribonucleic acid and demethylated CpG islands in the Bak promoter in hepatocellular carcinoma cells. Using the xenograft mouse tumor model, we demonstrated that zinc-binding protein-89 or inhibitors of either epigenetic enzymes could stimulate Bak expression, induce apoptosis, and arrest tumor growth and that the maximal effort was achieved when zinc-binding protein-89 and the enzyme inhibitors were used in combination. Conclusively, zinc-binding protein-89 upregulates the expression of Bak by targeting multiple components of the epigenetic pathway in hepatocellular carcinoma.

Indexed as

Epigenesis, GeneticAcetylationAnimalsApoptosisBase Sequencebcl-2 Homologous Antagonist-Killer ProteinCarcinoma, HepatocellularCell Line, TumorCell ProliferationCpG IslandsDNA-Binding ProteinsDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA MethylationDown-RegulationGene Expression Regulation, Neoplasticbcl-2 Homologous Antagonist-Killer ProteinDNA-Binding ProteinsDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesHistone Deacetylase 3Histone Deacetylase InhibitorsHistone DeacetylasesTranscription FactorsZNF148 protein, human5-aza-2′-deoxycytidine5-Aza-dCBakChIPchromatin immunoprecipitationco-immunoprecipitationCo-IPDNA methyltransferaseDNMTHCCHDAChepatocellular carcinomaHepatocellular carcinomahistone deacetylaseimmortalized non-tumorigenic hepatocyte cell lineMeCP2methyl-CpG-binding protein 2MIHAsodium valproic acidVPAZBP-89Zebuzebularine

Identifiers

PMID23954442
PMCPMC4160027
OpenAlexW2103457796

What OpenQuestion holds

Textmetadata
LicenceTDM
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.