Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9131993 | Genomics | 2005 | 14 Pages |
Abstract
Loss of heterozygosity on chromosome 22q13.31 is a frequent event during human breast and colorectal carcinogenesis. Herein we characterize a novel gene at chromosome 22q13.31 designated PRR5. Alternative promoter usage and splicing converge to generate five PRR5 transcript variants with maximum mRNA expression in kidney. In vitro transcription/translation demonstrated that the five variants generate three protein isoforms differing in their N-terminal length. Mutational analysis of PRR5 in human breast and colorectal tumors did not reveal somatic mutations. However, mRNA expression analyses revealed PRR5 overexpression in a majority of colorectal tumors but substantial downregulation of PRR5 expression in a subset of breast tumors and reduced expression in two breast cancer cell lines. Treatment with trichostatin A increased PRR5 mRNA levels in BT549 and MDA-MB-231 cells, whereas 5â²-aza-2â²-deoxycytidine induced expression in MDA-MB-231 cells only. Thus, PRR5 may represent a potential candidate tumor suppressor gene in breast cancer.
Keywords
PCR-SSCP analysisUTRCHTN5′-Aza-2′-deoxycytidineDMETSARACE-PCR5azadCRT-PCRq-PCRreverse transcriptase-PCRloss of heterozygosityESTTrichostatin AExpressed Sequence TagAlternative splicingCpG islandColorectal cancerBreast cancerLOHMethylationuntranslated regionquantitative real-time PCRProlineAlternative promoter
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Authors
Cameron N. Johnstone, Sergi CastellvÃ-Bel, Laura M. Chang, Raphael K. Sung, Mark J. Bowser, Josep M. Piqué, Antoni Castells, Anil K. Rustgi,