Hypermethylation of the cell cycle inhibitor p15INK4b 3′-untranslated region interferes with its transcriptional regulation in primary lymphomas View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1999-01-20

AUTHORS

Marcos Malumbres, Ignacio Pérez de Castro, Javier Santos, José Fernández Piqueras, Angel Pellicer

ABSTRACT

The cyclin-dependent kinase inhibitor p15INK4b has been shown to be involved in human and rodent tumors and seems to act as a tumor suppressor gene in hematological malignancies. Alterations of this gene in tumors include mainly homozygous deletions and hypermethylation of the CpG island in the promoter region. In this work, we describe a new area sensitive to methylation in the 3′ untranslated region (UTR) of the murine p15INK4b gene. This region shows different levels of methylation depending on the tissues, being relatively highly methylated in brain and gut, and weakly methylated in liver, spleen or thymus. DNA methylation and expression is similar in both maternal and paternal alleles indicating no imprinting effect. Although methylation of the p15INK4b 3′-UTR is low in normal thymus, increased levels (up to 100%) of specific methylation in this region are found in up to 30% of radiation- or carcinogen-induced thymic lymphomas, correlating with decreased gene expression. Hypermethylation of the p15INK4b 3′-UTR frequently occurs in tumors with loss of heterozygosity (LOH) but without methylation of the promoter CpG island or intragenic mutations. Furthermore, in vitro CpG methylation of the 3′-UTR produces reduced levels of a luciferase reporter in cultured cells. Methylation of two CpG sites in a 120 bp region is sufficient to interfere with transcription of the reporter gene. These data suggest that although the levels of p15INK4b in normal tissues can be mainly determined by promoter regulatory elements, strong hypermethylation of the 3′-UTR can interfere with transcription. Thus, hypermethylation of the 3′-UTR may explain the lack of p15INK4b gene expression in a subset of tumors with no promoter methylation and could be a new alternative mechanism for tumor suppressor gene inactivation in tumorigenesis. More... »

PAGES

385-396

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1202299

DOI

http://dx.doi.org/10.1038/sj.onc.1202299

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1037254525

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9927195


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104 promoter methylation
105 promoter region
106 promoter regulatory elements
107 radiation
108 reduced levels
109 region
110 regulation
111 regulatory elements
112 reporter
113 reporter gene
114 rodent tumors
115 sites
116 specific methylation
117 spleen
118 strong hypermethylation
119 subset
120 subset of tumors
121 suppressor gene
122 suppressor gene inactivation
123 thymic lymphomas
124 thymus
125 tissue
126 transcription
127 transcriptional regulation
128 tumor suppressor gene
129 tumor suppressor gene inactivation
130 tumorigenesis
131 tumors
132 untranslated region
133 work
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