ArticleCell death and differentiation2011
CASZ1, a candidate tumor-suppressor gene, suppresses neuroblastoma tumor growth through reprogramming gene expression.
Article in Cell death and differentiation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 97 citations in OpenAlex.
- Human papillomavirus and the landscape of secondary genetic alterations in oral cancers.Genome research · 2019Trial
- Tumor suppressor network dysregulation in neuroblastoma: molecular mechanisms and precision therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Letter to the editor: epigenetic regulation of casz1 and stratification of ccRCC treatment.International journal of surgery (London, England) · 2026Article
- Genome-Wide Association Study of Immune Indices in Yaks.Animals : an open access journal from MDPI · 2025Article
- Article
- Role of the CASZ1 transcription factor in tissue development and disease.European journal of medical research · 2023Review
- Review
- Zinc finger transcription factor CASZ1b is involved in the DNA damage response in live cells.Biochemical and biophysical research communications · 2023Article
- Fusion sequencing via terminator-assisted synthesis (FTAS-seq) identifies TMPRSS2 fusion partners in prostate cancer.Molecular oncology · 2023Article
- CASZ1 promotes migration, invasion, and metastasis of lung cancer cells by controlling expression of ITGAV.American journal of cancer research · 2023Article
- Transcription factor CASZ1 increases an oncogenic transcriptional process in tumorigenesis and progression of glioma cells.MedComm · 2022Article
- Loss of CASZ1 tumor suppressor linked to oncogenic subversion of neuroblastoma core regulatory circuitry.Cell death & disease · 2022Article
- Upregulation of p75NTR by Histone Deacetylase Inhibitors Sensitizes Human Neuroblastoma Cells to Targeted Immunotoxin-Induced Apoptosis.International journal of molecular sciences · 2022Article
- Allele-specific expression reveals genes with recurrent cis-regulatory alterations in high-risk neuroblastoma.Genome biology · 2022Article
- Genistein as a regulator of signaling pathways and microRNAs in different types of cancers.Cancer cell international · 2021Review
- CASZ1b is a novel transcriptional corepressor of mineralocorticoid receptor.Hypertension research : official journal of the Japanese Society of Hypertension · 2021Article
- Circular RNA circANKRD36 regulates Casz1 by targeting miR-599 to prevent osteoarthritis chondrocyte apoptosis and inflammation.Journal of cellular and molecular medicine · 2021Article
- Valproic acid upregulates the expression of the p75NTR/sortilin receptor complex to induce neuronal apoptosis.Apoptosis : an international journal on programmed cell death · 2020Article
- CASZ1 induces skeletal muscle and rhabdomyosarcoma differentiation through a feed-forward loop with MYOD and MYOG.Nature communications · 2020Article
- Aberrant Methylation and Differential Expression of SLC2A1, TNS4, GAPDH, ATP8A2, and CASZ1 Are Associated with the Prognosis of Lung Adenocarcinoma.BioMed research international · 2020Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
Neuroblastoma (NB) is a common childhood malignant tumor of the neural crest-derived sympathetic nervous system. In NB the frequent loss of heterozygosity (LOH) on chromosome 1p raises the possibility that this region contains tumor-suppressor genes whose inactivation contributes to tumorigenesis. The human homolog of the Drosophila neural fate determination gene CASZ1, a zinc-finger transcription factor, maps to chromosome 1p36.22, a region implicated in NB tumorigenesis. Quantitative real-time PCR analysis showed that low-CASZ1 expression is significantly correlated with increased age (≥18 months), Children's Oncology Group high-risk classification, 1p LOH and MYCN amplification (all P<0.0002) and decreased survival probability (P=0.0009). CASZ1 was more highly expressed in NB with a differentiated histopathology (P<0.0001). Retinoids and epigenetic modification agents associated with regulation of differentiation induced CASZ1 expression. Expression profiling analysis revealed that CASZ1 regulates the expression of genes involved in regulation of cell growth and developmental processes. Specific restoration of CASZ1 in NB cells induced cell differentiation, enhanced cell adhesion, inhibited migration and suppressed tumorigenicity. These data are consistent with CASZ1 being a critical modulator of neural cell development, and that somatically acquired disruption of normal CASZ1 expression contributes to the malignant phenotype of human NB.
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