NDLI: Promoter methylation study of the H37/RBM5 tumor suppressor gene from the 3p21.3 human lung cancer tumor suppressor locus

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Promoter methylation study of the H37/RBM5 tumor suppressor gene from the 3p21.3 human lung cancer tumor suppressor locus

Content Provider	Springer Nature Link
Author	Oh, Juliana J. Boctor, Baher N. Jimenez, Cynthia A. Lopez, Roberto Koegel, Ashley K. Taschereau, Eileen O. Phan, Diana T. Jacobsen, Steven E. Slamon, Dennis J.
Copyright Year	2007
Abstract	Loss of heterozygosity (LOH) at chromosome 3p21.3 is one of the most prevalent genetic disturbances occurring at the earliest stage of tumor development for a wide variety of human cancers, culminated in lung cancer. The 19 genes residing at 3p21.3 have been vigorously characterized for tumor suppressor activity and gene inactivation mechanism because of their potentially significant merits of clinical applications. Many of these 19 genes have been shown to manifest various growth inhibitory properties, however none of them are inactivated by coding mutations in their remaining allele as in the Knudson’s two- hits hypothesis. Thus far the most prevailing, alternative gene inactivation mechanism known for the 3p21.3 TSGs is epigenetic silencing by promoter hypermethylation. Previously, we have focused our investigation on one of the 19 genes at 3p21.3, H37/RBM5, and demonstrated its tumor suppressor activity both in vitro and in vivo as well as its mRNA/protein expression loss from the remaining allele in a majority of the primary lung tumors examined. The current study tested our hypothesis that the H37 inactivation in primary lung tumors may, as seen in most of the other 3p21.3 TSGs, be due to hypermethylation in its promoter CpG islands. Contrary to this most plausible postulation, however, we found no evidence of epigenetic gene silencing for the H37 TSG. Here we suggest some of the possible, further- alternative means of the H37 gene expression loss in tumor, including defects in transcription and post-transcriptional/translational modifications as well as mechanisms related to haploinsufficiency.
Starting Page	55
Ending Page	64
Page Count	10
File Format	PDF
ISSN	03406717
Journal	Human Genetics
Volume Number	123
Issue Number	1
e-ISSN	14321203
Language	English
Publisher	Springer-Verlag
Publisher Date	2007-11-22
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Metabolic Diseases Internal Medicine Molecular Medicine Human Genetics
Content Type	Text
Resource Type	Article
Subject	Genetics Genetics (clinical)

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