3-Deazaneplanocin A - CAS 102052-95-9
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Not Intended for Therapeutic Use. For research use only.
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3-Deazaneplanocin A (DZNep), an inhibitor of S-adenosylmethionine-dependent methyltransferase that targets the degradation of EZH2.
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1.3-Deazaneplanocin A suppresses aggressive phenotype-related gene expression in an oral squamous cell carcinoma cell line.
Hatta M1, Naganuma K2, Kato K3, Yamazaki J3. Biochem Biophys Res Commun. 2015 Dec 4-11;468(1-2):269-73. doi: 10.1016/j.bbrc.2015.10.115. Epub 2015 Oct 23.
In tumor tissues, alterations of gene expression caused by aberrant epigenetic modifications confer phenotypic diversity on malignant cells. Although 3-deazaneplanocin A (DZNep) has been shown to reactivate tumor suppressor genes in several cancer cells, it remains unclear whether DZNep attenuates the malignant phenotypes of oral squamous cell carcinoma (OSCC) cells. In this study, we investigated the effect of DZNep on the expression of genes related to aggressive phenotypes, such as epithelial-mesenchymal transition, in OSCC cells. We found that DZNep reduced the cellular levels of polycomb group proteins (EZH2, SUZ12, BMI1, and RING1A) and the associated trimethylation of Lys27 on histone H3 and monoubiquitination of Lys119 on histone H2A in the poorly differentiated OSCC cell line SAS. Immunocytochemical staining demonstrated that DZNep induced the reorganization of filamentous actin and the membrane localization of E-cadherin associated with cell-cell adhesions.
2.Growth Inhibition Accompanied by MOB1 Upregulation in Human Acute Lymphoid Leukemia Cells by 3-Deazaneplanocin A.
Shen J1, Su J, Wu D, Zhang F, Fu H, Zhou H, Xu M. Biochem Genet. 2015 Oct;53(9-10):268-79. doi: 10.1007/s10528-015-9688-7. Epub 2015 Aug 23.
Our purpose was to investigate the effect of 3-deazaneplanocin A (DZNep) on human T-cell acute lymphoid leukemia (T-ALL) cells, and to explore the underlying molecular mechanisms. The human T-ALL cell line Molt4 was treated with DZNep, and cell proliferation was examined. The expression of Mps one binder kinase activator 1 gene (MOB1) mRNA and protein was determined by RT-PCR and Western blotting, respectively. The histone modification effect of DZNep on the lysine 9 of histone 3 associated with MOB1 promoters was examined with chromatin immunoprecipitation and quantitative PCR, and CpG methylation in MOB1 promoters was detected by bisulfite sequencing PCR. DZNep treatment inhibited the growth of Molt4 cells. The expressions of MOB1 genes were upregulated by DZNep treatment, and histone methylations in their promoters were significantly reduced. The results indicate that DZNep is a promising therapeutic compound for the treatment of human T-ALL.
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CAS 102052-95-9 3-Deazaneplanocin A

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