ArticleMolecular and cellular biology2012
Characterization of critical domains within the tumor suppressor CASZ1 required for transcriptional regulation and growth suppression.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Human papillomavirus and the landscape of secondary genetic alterations in oral cancers.Genome research · 2019Trial
- Role of the CASZ1 transcription factor in tissue development and disease.European journal of medical research · 2023Review
- Review
- CASZ1 promotes migration, invasion, and metastasis of lung cancer cells by controlling expression of ITGAV.American journal of cancer research · 2023Article
- Identification of a Novel de Novo Variant in the CASZ1 Causing a Rare Type of Dilated Cardiomyopathy.International journal of molecular sciences · 2022Article
- Loss of CASZ1 tumor suppressor linked to oncogenic subversion of neuroblastoma core regulatory circuitry.Cell death & disease · 2022Article
- Mutations of 1p genes do not consistently abrogate tumor suppressor functions in 1p-intact neuroblastoma.BMC cancer · 2022Article
- CASZ1 induces skeletal muscle and rhabdomyosarcoma differentiation through a feed-forward loop with MYOD and MYOG.Nature communications · 2020Article
- The Prognostic Significance of Protein Expression of CASZ1 in Clear Cell Renal Cell Carcinoma.Disease markers · 2019Article
- Cell-free plasma hypermethylated CASZ1, CDH13 and ING2 are promising biomarkers of esophageal cancer.Journal of biomedical research · 2018Article
- Formation of a TBX20-CASZ1 protein complex is protective against dilated cardiomyopathy and critical for cardiac homeostasis.PLoS genetics · 2017Article
- Identification of CASZ1 NES reveals potential mechanisms for loss of CASZ1 tumor suppressor activity in neuroblastoma.Oncogene · 2017Article
- Regulation of cancer epigenomes with a histone-binding synthetic transcription factor.NPJ genomic medicine · 2017Article
- Zinc finger transcription factor CASZ1 interacts with histones, DNA repair proteins and recruits NuRD complex to regulate gene transcription.Oncotarget · 2015Article
- Essential role of the zinc finger transcription factor Casz1 for mammalian cardiac morphogenesis and development.The Journal of biological chemistry · 2014Article
- Differential regulation of CASZ1 protein expression during cardiac and skeletal muscle development.Developmental dynamics : an official publication of the American Association of Anatomists · 2014Article
- Switching metal ion coordination and DNA Recognition in a Tandem CCHHC-type zinc finger peptide.Inorganic chemistry · 2013Article
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
CASZ1 is a zinc finger (ZF) transcription factor that is critical for controlling the normal differentiation of subtypes of neural and cardiac muscle cells. In neuroblastoma tumors, loss of CASZ1 is associated with poor prognosis and restoration of CASZ1 function suppresses neuroblastoma tumorigenicity. However, the key domains by which CASZ1 transcription controls developmental processes and neuroblastoma tumorigenicity have yet to be elucidated. In this study, we show that loss of any one of ZF1 to ZF4 resulted in a 58 to 79% loss in transcriptional activity, as measured by induction of tyrosine hydroxylase promoter-luciferase activity, compared to that of wild-type (WT) CASZ1b. Mutation of ZF5 or deletion of the C-terminal sequence of amino acids (aa) 728 to 1166 (a truncation of 38% of the protein) does not significantly alter transcriptional function. A series of N-terminal truncations reveals a critical transcriptional activation domain at aa 31 to 185 and a nuclear localization signal at aa 23 to 29. Soft agar colony formation assays and xenograft studies show that WT CASZ1b is more active in suppressing neuroblastoma growth than CASZ1b with a ZF4 mutation or a deletion of aa 31 to 185. This study identifies key domains needed for CASZ1b to regulate gene transcription. Furthermore, we establish a link between loss of CASZ1b transcriptional activity and attenuation of CASZ1b-mediated inhibition of neuroblastoma growth and tumorigenicity.
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