Modulation of RIZ gene expression is associated to estradiol control of MCF-7 breast cancer cell proliferation

Gazzerro, Patrizia; Abbondanza, Ciro; D'Arcangelo, Andrea; Rossi, Mariangela; Medici, Nicola; Moncharmont, Bruno; Puca, Giovanni Alfredo

doi:10.1016/j.yexcr.2005.11.002

Cited by 34 publications

(49 citation statements)

References 32 publications

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“…Until the introduction of luteinizing hormone-releasing hormone agonist therapy, estrogen therapy was often used for hormonal manipulation of PCa. (34) Because estradiol treatment produces a selective decrease in RIZ1 expression, (35) it is interesting to investigate the RIZ1 expression in PCa tissues from patients who received preoperative hormone treatment.…”

Section: Discussionmentioning

confidence: 99%

DNA methylation of the RIZ1 gene is associated with nuclear accumulation of p53 in prostate cancer

et al. 2006

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The retinoblastoma protein-interacting zinc finger gene, RIZ1, is thought to be a tumor suppressor gene. RIZ1 is inactivated by mutation, deletion and DNA methylation in several human cancers. In the present study, the relationship between DNA methylation of RIZ1 and mutation of p53 was investigated in prostate cancer (PCa). In total, 47 cases of node-negative PCa (stages I-III) were analyzed. DNA methylation of the RIZ1 gene was detected in 20 (42.6%) of the 47 PCa tissues by methylation-specific polymerase chain reaction. DNA methylation of the RIZ1 gene was not associated with clinicopathological features. DNA methylation of RIZ1 tended to be present more frequently in PCa specimens with a high Gleason score (16/30, 53.3%) than in those with a low Gleason score (4/17, 23.5%); however, this tendency was not statistically significant (P = 0.0675). Nuclear accumulation of p53 was observed in four (8.5%) of 47 PCa specimens by immunostaining. All four PCa specimens with nuclear accumulation of p53 were stage III disease and showed DNA methylation of RIZ1. However, of the remaining 43 cancers without nuclear accumulation of p53, DNA methylation of RIZ1 was observed in only 16 (37.2%) specimens (P = 0.0272). Of the three PCa cell lines, only the PC3 cell line showed loss of RIZ1 mRNA due to DNA methylation, and this loss was rectified by treatment with a demethylating agent, 5-Aza-2′ ′ ′ ′-deoxycytidine. These results suggest that transcriptional inactivation of RIZ1 by aberrant DNA methylation may contribute to prostate carcinogenesis. Genetic alterations are likely associated with epigenetic alterations in PCa. (Cancer Sci 2007; 98: 32-36) P rostate cancer (PCa) is one of the most common cancers and the second leading cause of cancer death in men in the USA.(1) An understanding of the genetic and epigenetic pathways involved in the pathogenesis of PCa is essential for development of improved diagnostic and treatment modalities. A variety of genetic and epigenetic alterations are associated with PCa. (2,3) Epigenetic changes, such as DNA methylation of CpG islands, are detected commonly in human cancers. Hypermethylation of CpG islands is associated with silencing of many genes, especially defective tumor-related genes, and has been proposed as an alternative way to inactivate tumor-related genes in human cancers.(4,5) Identification of methylated genes may be useful in the diagnosis and treatment of PCa and may provide insight into prostate carcinogenesis. Prior studies have shown that DNA hypermethylation is a crucial mechanism in transcriptional silencing of tumor-related genes in PCa. (6,7) The retinoblastoma protein-interacting zinc finger gene, RIZ1, was isolated with a functional screen for retinoblastoma (Rb)-binding proteins.(8) Domain analysis suggested that RIZ1 is a histone methyltransferase (HMT) specific for the lysine 9 residue of histone H3, an activity known to be linked with transcriptional repression.(9) RIZ1 is considered to be a tumor suppressor gene because it can induce G 2 -M arrest and apo...

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Section: Discussionmentioning

confidence: 99%

DNA methylation of the RIZ1 gene is associated with nuclear accumulation of p53 in prostate cancer

et al. 2006

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“…Human PRDM2 (also known as RIZ1) is a strong tumor suppressor that induces G2/M cell cycle arrest and/or apoptosis in various tumor cells (6,9,10). Its PR domain can methylate histone H3 lysine 9 (H3K9) and is necessary in the repression of estrogen signaling genes (3,11).…”

Section: Introductionmentioning

confidence: 99%

Expression patterns of PRDM10 during mouse embryonic development

Park

Kim

2010

BMB Reports

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It is well known that PR/SET family members participate in transcriptional regulation via chromatin remodeling. PRDM10 might play an essential role in gene expression, but no such evidence has been observed so far. To assess PRDM10 expression at various stages of mouse development, we performed immunohistochemistry using available PRDM10 antibody. Embryos were obtained from three distinct developmental stages. At E8.5, PRDM10 expression was concentrated in the mesodermal and neural crest populations. As embryogenesis proceeded further to E13.5, PRMD10 expression was mainly in mesoderm-derived tissues such as somites and neural crest-derived populations such as the facial skeleton. This expression pattern was consistently maintained to the fetal growth period E16.5 and adult mouse, suggesting that PRDM10 may function in tissue differentiation. Our study revealed that PRDM10 might be a transcriptional regulator for normal tissue differentiation during mouse embryonic development. [BMB reports 2010; 43(1): 29-33]

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“…2A) is E 2 -sensitive. 22 Analysis of RIZ gene produced equally interesting results. The captured promoter 2 specifically associated, in fact, with increased amounts (60-70%) of molecules from exons 9a and 10 (where alternative polyA addition occurs) after hormone challenge and, as opposite, a decreased recovery of the E 2 -insensitive promoter (promoter 1) could be monitored (Fig.…”

Section: Cellsmentioning

confidence: 97%