Evidence map›Paper›PMID 39266576›Full record

ArticleScientific reports2024

Epigenetic silencing of ZIC4 unveils a potential tumor suppressor role in pediatric choroid plexus carcinoma.

Dina Hesham, Amal Mosaab, Nada Amer, Nouran Al-Shehaby, Sameh Magdeldin, Ahmed Hassan, Hristo Georgiev, Hisham Elshoky, Mona Rady, Khaled Abou Aisha and 2 more

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
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  4. Review
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  6. 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

12 authors.

Dina HeshamTumor Biology Research Program, Basic Research Unit, Research Department, Children's Cancer Hospital in Egypt 57357, 1 Sekket El Emam, El Madbah El Kadeem Yard, Sayeda Zeinab, Cairo, Egypt.
Amal MosaabTumor Biology Research Program, Basic Research Unit, Research Department, Children's Cancer Hospital in Egypt 57357, 1 Sekket El Emam, El Madbah El Kadeem Yard, Sayeda Zeinab, Cairo, Egypt.
Nada AmerTumor Biology Research Program, Basic Research Unit, Research Department, Children's Cancer Hospital in Egypt 57357, 1 Sekket El Emam, El Madbah El Kadeem Yard, Sayeda Zeinab, Cairo, Egypt.
Nouran Al-ShehabyTumor Biology Research Program, Basic Research Unit, Research Department, Children's Cancer Hospital in Egypt 57357, 1 Sekket El Emam, El Madbah El Kadeem Yard, Sayeda Zeinab, Cairo, Egypt.
Sameh MagdeldinProteomics and Metabolomics Research Program, Basic Research Unit, Research Department, Children's Cancer Hospital Egypt 57357, Cairo, Egypt.
Ahmed HassanInstitute of Immunology, Hannover Medical School, Hannover, Germany.
Hristo GeorgievInstitute of Immunology, Hannover Medical School, Hannover, Germany.
Hisham ElshokyTumor Biology Research Program, Basic Research Unit, Research Department, Children's Cancer Hospital in Egypt 57357, 1 Sekket El Emam, El Madbah El Kadeem Yard, Sayeda Zeinab, Cairo, Egypt.
Mona RadyMicrobiology, Immunology and Biotechnology Department, Faculty of Pharmacy and Biotechnology, German University in Cairo (GUC), Cairo, Egypt.
Khaled Abou AishaMicrobiology, Immunology and Biotechnology Department, Faculty of Pharmacy and Biotechnology, German University in Cairo (GUC), Cairo, Egypt.
Ola SabetTumor Biology Research Program, Basic Research Unit, Research Department, Children's Cancer Hospital in Egypt 57357, 1 Sekket El Emam, El Madbah El Kadeem Yard, Sayeda Zeinab, Cairo, Egypt.
Shahenda El-NaggarTumor Biology Research Program, Basic Research Unit, Research Department, Children's Cancer Hospital in Egypt 57357, 1 Sekket El Emam, El Madbah El Kadeem Yard, Sayeda Zeinab, Cairo, Egypt. shahenda.elnaggar@57357.org.ORCID 0000-0001-6465-9881

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zic family member ZIC4 is a transcription factor that has been shown to be silenced in several cancers. However, understanding the regulation and function of ZIC4 in pediatric choroid plexus tumors (CPTs) remained limited. This study employed data mining and bioinformatics analysis to investigate the DNA methylation status of ZIC4 in CPTs and its correlation with patient survival. Our results unveiled ZIC4 methylation as a segregating factor, dividing CPT cohorts into two clusters, with hyper-methylation linked to adverse prognosis. Hyper-methylation of ZIC4 was confirmed in a choroid plexus carcinoma-derived cell line (CCHE-45) by bisulfite sequencing. Furthermore, our study demonstrated that demethylating agent and a histone methyltransferase inhibitor could reverse ZIC4 silencing. RNA sequencing and proteomic analysis showed that ZIC4 over-expression influenced genes and proteins involved in immune response, antigen processing and presentation, endoplasmic reticulum stress, and metabolism. Functionally, re-expressing ZIC4 negatively impacted cell proliferation and migration. Ultimately, these findings underscore ZIC4 hyper-methylation as a prognostic marker in CPTs and shed light on potential mechanisms underlying its tumor suppressor role in CPC. This insight paves the way for novel therapeutic targets in treating aggressive CPTs.

Indexed as

Choroid Plexus NeoplasmsDNA MethylationEpigenesis, GeneticGene Expression Regulation, NeoplasticTranscription FactorsCarcinomaCell Line, TumorCell MovementCell ProliferationChildChild, PreschoolFemaleGene SilencingGenes, Tumor SuppressorHumansInfantNerve Tissue ProteinsTranscription FactorsZIC4 protein, humanEpigenetic silencingPediatric choroid plexus carcinomaProteomic profilingTranscriptomic profilingTumor suppressorZIC4

Identifiers

PMID39266576
PMCPMC11393135

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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.