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The PVT‐1 oncogene is a Myc protein target that is overexpressed in transformed cells
Author(s) -
Carramusa Letizia,
Contino Flavia,
Ferro Arianna,
Minafra Luigi,
Perconti Giovanni,
Giallongo Agata,
Feo Salvatore
Publication year - 2007
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.21133
Subject(s) - biology , chromatin immunoprecipitation , microbiology and biotechnology , gene , transfection , chromatin , gene expression , neuroblastoma , n myc , oncogene , reporter gene , transcription (linguistics) , regulation of gene expression , transcription factor , chromosomal translocation , immunoprecipitation , promoter , cell culture , genetics , cell cycle , linguistics , philosophy , ganglioneuroma
The human PVT‐1 gene is located on chromosome 8 telomeric to the c‐Myc gene and it is frequently involved in the translocations occurring in variant Burkitt's lymphomas and murine plasmacytomas. It has been proposed that PVT‐1 regulates c‐Myc gene transcription over a long distance. To get new insights into the functional relationships between the two genes, we have investigated PVT‐1 and c‐Myc expression in normal human tissues and in transformed cells. Our findings indicate that PVT‐1 expression is restricted to a relative low number of normal tissues compared to the wide distribution of c‐Myc mRNA, whereas the gene is highly expressed in many transformed cell types including neuroblastoma cells that do not express c‐Myc. Reporter gene assays were used to dissect the PVT‐1 promoter and to identify the region responsible for the elevated expression observed in transformed cells. This region contains two putative binding sites for Myc proteins. The results of transfection experiments in RAT1‐MycER cells and chromatin immunoprecipitation (ChIP) assays in proliferating and differentiated neuroblastoma cells indicate that PVT‐1 is a downstream target of Myc proteins. J. Cell. Physiol. 213: 511–518, 2007. © 2007 Wiley‐Liss, Inc.