Evidence map›Paper›PMID 24459426›Full record

ArticleTheScientificWorldJournal2013

Association of self-DNA mediated TLR9-related gene, DNA methyltransferase, and cytokeratin protein expression alterations in HT29-cells to DNA fragment length and methylation status.

István Fűri, Ferenc Sipos, Sándor Spisák, Gergő Kiszner, Barnabás Wichmann, Andrea Schöller, Zsolt Tulassay, Györgyi Műzes, Béla Molnár

Open access · goldAbstract read
In one paragraph

Article in TheScientificWorldJournal, 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
0.6field-weighted citation impact, top 30% 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, 14 citations in OpenAlex.

  1. T cell-intrinsic PRR signaling in immunity and pathology.Acta biochimica et biophysica Sinica · 2026
    Review
  2. Review
  3. Review
  4. Article
  5. Survival of HT29 Cancer Cells Is Affected by IGF1R InhibitionPathology oncology research : POR · 2022
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
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 2 institutions in 1 country.

István Fűri2nd Department of Internal Medicine, Semmelweis University, Szentkirályi Street 46, Budapest 1088, Hungary.
Ferenc Sipos2nd Department of Internal Medicine, Semmelweis University, Szentkirályi Street 46, Budapest 1088, Hungary.
Sándor SpisákMolecular Medicine Research Unit, Hungarian Academy of Sciences, Nádor Street 7, Budapest 1051, Hungary.
Gergő Kiszner1st Department of Pathology and Experimental Oncology, Semmelweis University, Üllői Street 26, Budapest 1085, Hungary.
Barnabás Wichmann2nd Department of Internal Medicine, Semmelweis University, Szentkirályi Street 46, Budapest 1088, Hungary.
Andrea Schöller2nd Department of Internal Medicine, Semmelweis University, Szentkirályi Street 46, Budapest 1088, Hungary.
Zsolt TulassayMolecular Medicine Research Unit, Hungarian Academy of Sciences, Nádor Street 7, Budapest 1051, Hungary.
Györgyi Műzes2nd Department of Internal Medicine, Semmelweis University, Szentkirályi Street 46, Budapest 1088, Hungary.
Béla MolnárMolecular Medicine Research Unit, Hungarian Academy of Sciences, Nádor Street 7, Budapest 1051, Hungary.
Semmelweis University · HUHungarian Academy of Sciences · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To understand the biologic role of self-DNA bound to Toll-like Receptor 9 (TLR9), we assayed its effect on gene and methyltransferase expressions and cell differentiation in HT29 cells. HT29 cells were incubated separately with type-1 (normally methylated/nonfragmented), type-2 (normally methylated/fragmented), type-3 (hypermethylated/nonfragmented), or type-4 (hypermethylated/fragmented) self-DNAs. Expression levels of TLR9-signaling and proinflammatory cytokine-related genes were assayed by qRT-PCR. Methyltransferase activity and cell differentiation were examined by using DNA methyltransferase (DNMT1, -3A, -3B) and cytokeratin (CK) antibodies. Treatment with type-1 DNA resulted in significant increase in TLR9 expression. Type-2 treatment resulted in the overexpression of TLR9-related signaling molecules (MYD88A, TRAF6) and the IL8 gene. In the case of type-3 treatment, significant overexpression of NFkB, IRAK2, and IL8 as well as downregulation of TRAF6 was detected. Using type-4 DNA, TRAF6 and MYD88A gene expression was upregulated, while MYD88B, IRAK2, IL8, and TNFSF10 were all underexpressed. CK expression was significantly higher only after type-1 DNA treatment. DNMT3A expression could also be induced by type-1 DNA treatment. DNA structure may play a significant role in activation of the TLR9-dependent and even independent proinflammatory pathways. There may be a molecular link between TLR9 signaling and DNMT3A. The mode of self-DNA treatment may influence HT29 cell differentiation.

Indexed as

Cell DifferentiationCell Line, TumorDNADNA (Cytosine-5-)-MethyltransferasesDNA MethylationGene Expression RegulationHumansInterleukin-1 Receptor-Associated KinasesInterleukin-8KeratinsMyeloid Differentiation Factor 88NF-kappa BTNF Receptor-Associated Factor 6TNF-Related Apoptosis-Inducing LigandToll-Like Receptor 9CXCL8 protein, humanDNADNA (Cytosine-5-)-MethyltransferasesInterleukin-1 Receptor-Associated KinasesInterleukin-8IRAK3 protein, humanKeratinsMYD88 protein, humanMyeloid Differentiation Factor 88NF-kappa BTLR9 protein, humanTNF Receptor-Associated Factor 6TNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanToll-Like Receptor 9

Identifiers

PMID24459426
PMCPMC3891537
OpenAlexW2128282610

What OpenQuestion 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 OpenQuestion graph.