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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.

Overexpression of Full-Length ETV1 Transcripts in Clinical Prostate Cancer Due to Gene Translocation