ArticleMedical oncology (Northwood, London, England)2017
ZAR1 knockdown promotes the differentiation of human neuroblastoma cells by suppression of MYCN expression.
Article in Medical oncology (Northwood, London, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- ZAR1/2-Regulated Epigenetic Modifications are Essential for Age-Associated Oocyte Quality Maintenance and Zygotic Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Skeletal muscle transcriptional networks linked to type I myofiber grouping in Parkinson's disease.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Calreticulin regulates MYCN expression to control neuronal differentiation and stemness of neuroblastoma.Journal of molecular medicine (Berlin, Germany) · 2019Article
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although DNA hypermethylation at non-promoter region of the Zygote arrest 1 (ZAR1) gene has been observed in many types of tumor, including neuroblastoma (NB), the role of this gene in tumor development and/or progression is unclear. One reason is that knowledge about the function of ZAR1 protein is limited. Although it has been reported that ZAR1 plays a crucial role in early embryogenesis and may act as a transcriptional repressor for some transcripts, the detailed mechanism is still elusive. In the present study, we analyzed public data of NB patients and found that higher expression levels of ZAR1 were significantly associated with a shorter survival period. Consistent with this result, ZAR1-depleted NB cells showed well-differentiated phenotypes with elongated neurites and upregulated expression of TRKA and RET, which are markers for differentiated NB. Moreover, the expression level of MYCN protein was markedly suppressed in ZAR1-depleted NB cells. MYCN-depleted cells showed similar phenotypes to ZAR1-depleted cells. The present findings indicate that ZAR1 has oncogenic effects in NB by suppressing cell differentiation via regulation of MYCN expression.
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