We performed methylation specific PCR analysis on the RIZ1 promoter in MDS and AML. Methylation was detected in 17 of 34 MDS (50%) and 22 of 72 AML (31%) (p=0.053). Methylation was detected in eleven of 17 secondary AML from MDS (65%), and eleven of 55 de novo AML (20%) (p=0.0005). Bisulfite sequence revealed methylation at many CpG sites in the promoter. Decreased RIZ1 expression was accompanied by methylation in six of nine samples examined, while it was also observed in seven of 13 without methylation. Treatment of AML cells, that have RIZ1 methylation, with 5-Aza-dC, induced growth suppression with RIZ1 restoration. Our results suggest that the RIZ1 gene is inactivated in MDS and AML in part by methylation, whereas another mechanism should be involved in others.
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http://dx.doi.org/10.1016/j.leukres.2010.08.002 | DOI Listing |
Redox Biol
December 2024
Department of Emergency and Critical Care Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China; Emergency Medicine and Difficult Diseases Institute, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China; Department of Nephrology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China; Furong Laboratory, Changsha, Hunan, China. Electronic address:
Acute kidney injury (AKI) constitutes a significant public health issue. Sepsis accounts for over 50 % of AKI cases in the ICU. Recent findings from our research indicated that the PRD1-BF1-RIZ1 homeodomain protein 16 (PRDM16) inhibited the progression of diabetic kidney disease (DKD).
View Article and Find Full Text PDFMol Metab
November 2024
Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan. Electronic address:
Objective: Brown adipose tissue (BAT) plays an important role in mammalian thermogenesis through the expression of uncoupling protein 1 (UCP1). Our previous study identified cytoplasmic polyadenylation element binding protein 2 (CPEB2) as a key regulator that activates the translation of Ucp1 with a long 3'-untranslated region (Ucp1L) in response to adrenergic signaling. Mice lacking CPEB2 or Ucp1L exhibited reduced UCP1 expression and impaired thermogenesis; however, only CPEB2-null mice displayed obesogenic phenotypes.
View Article and Find Full Text PDFSci Rep
July 2024
Department of Neurological Surgery, University of California, San Francisco, San Francisco, CA, USA.
SNCAIP duplication may promote Group 4 medulloblastoma via induction of PRDM6, a poorly characterized member of the PRDF1 and RIZ1 homology domain-containing (PRDM) family of transcription factors. Here, we investigated the function of PRDM6 in human hindbrain neuroepithelial stem cells and tested PRDM6 as a driver of Group 4 medulloblastoma. We report that human PRDM6 localizes predominantly to the nucleus, where it causes widespread repression of chromatin accessibility and complex alterations of gene expression patterns.
View Article and Find Full Text PDFJ Transl Med
October 2023
Department of Precision Medicine, University of Campania "Luigi Vanvitelli", Naples, Italy.
Background: Colorectal cancer (CRC) is the third most deadly and fourth most diagnosed cancer worldwide. Despite the progress in early diagnosis and advanced therapeutic options, CRC shows a poor prognosis with a 5 year survival rate of ~ 45%. PRDM2/RIZ, a member of PR/SET domain family (PRDM), expresses two main molecular variants, the PR-plus isoform (RIZ1) and the PR-minus (RIZ2).
View Article and Find Full Text PDFduplication may promote Group 4 medulloblastoma induction of PRDM6, a poorly characterized member of the (PRDM) family of transcription factors. Here, we investigated the function of PRDM6 in human hindbrain neuroepithelial stem cells and tested PRDM6 as a driver of Group 4 medulloblastoma. We report that human PRDM6 localizes predominantly to the nucleus, where it causes widespread repression of chromatin accessibility and complex alterations of gene expression patterns.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!