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Overexpression of full-length ETV1 transcripts in clinical prostate cancer due to gene translocation.

Gasi, Delila, 1982 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper,Institute of Clinical Sciences
van der Korput, Hetty A (författare)
Douben, Hannie C (författare)
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de Klein, Annelies (författare)
de Ridder, Corrina M (författare)
van Weerden, Wytske M (författare)
Trapman, Jan (författare)
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2011
2011
Engelska.
Ingår i: PloS one. - 1932-6203. ; 6:1
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • ETV1 is overexpressed in a subset of clinical prostate cancers as a fusion transcript with many different partners. However, ETV1 can also be overexpressed as a full-length transcript. Full-length ETV1 protein functions differently from truncated ETV1 produced by fusion genes. In this study we describe the genetic background of full-length ETV1 overexpression and the biological properties of different full-length ETV1 isoforms in prostate cancer. Break-apart FISH showed in five out of six patient samples with overexpression of full-length ETV1 a genomic rearrangement of the gene, indicating frequent translocation. We were able to study the rearrangements in more detail in two tumors. In the first tumor 5'-RACE on cDNA showed linkage of the complete ETV1 transcript to the first exon of a prostate-specific two exon ncRNA gene that maps on chromosome 14 (EST14). This resulted in the expression of both full-length ETV1 transcripts and EST14-ETV1 fusion transcripts. In chromosome spreads of a xenograft derived from the second prostate cancer we observed a complex ETV1 translocation involving a chromosome 7 fragment that harbors ETV1 and fragments of chromosomes 4 and 10. Further studies revealed the overexpression of several different full-length transcripts, giving rise to four protein isoforms with different N-terminal regions. Even the shortest isoform synthesized by full-length ETV1 stimulated in vitro anchorage-independent growth of PNT2C2 prostate cells. This contrasts the lack of activity of even shorter N-truncated ETV1 produced by fusion transcripts. Our findings that in clinical prostate cancer overexpression of full-length ETV1 is due to genomic rearrangements involving different chromosomes and the identification of a shortened biologically active ETV1 isoform are highly relevant for understanding the mechanism of ETV1 function in prostate cancer.

Nyckelord

Chromosomes
Human
DNA-Binding Proteins
genetics
Gene Expression Regulation
Neoplastic
Humans
Male
Prostatic Neoplasms
genetics
Protein Isoforms
RNA
Neoplasm
analysis
Transcription Factors
genetics
Translocation
Genetic

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