SLC45A3-ELK4 is a novel and frequent erythroblast transformation-specific fusion transcript in prostate cancer

Cancer Res. 2009 Apr 1;69(7):2734-8. doi: 10.1158/0008-5472.CAN-08-4926. Epub 2009 Mar 17.

Abstract

Chromosomal rearrangements account for all erythroblast transformation-specific (ETS) family member gene fusions that have been reported in prostate cancer and have clinical, diagnostic, and prognostic implications. Androgen-regulated genes account for the majority of the 5' genomic regulatory promoter elements fused with ETS genes. TMPRSS2-ERG, TMPRSS2-ETV1, and SLC45A3-ERG rearrangements account for roughly 90% of ETS fusion prostate cancer. ELK4, another ETS family member, is androgen regulated, involved in promoting cell growth, and highly expressed in a subset of prostate cancer, yet the mechanism of ELK4 overexpression is unknown. In this study, we identified a novel ETS family fusion transcript, SLC45A3-ELK4, and found it to be expressed in both benign prostate tissue and prostate cancer. We found high levels of SLC45A3-ELK4 mRNA restricted to a subset of prostate cancer samples. SLC45A3-ELK4 transcript can be detected at high levels in urine samples from men at risk for prostate cancer. Characterization of the fusion mRNA revealed a major variant in which SLC45A3 exon 1 is fused to ELK4 exon 2. Based on quantitative PCR analyses of DNA, unlike other ETS fusions described in prostate cancer, the expression of SLC45A3-ELK4 mRNA is not exclusive to cases harboring a chromosomal rearrangement. Treatment of LNCaP cancer cells with a synthetic androgen (R1881) revealed that SLC45A3-ELK4, and not endogenous ELK4, mRNA expression is androgen regulated. Altogether, our findings show that SLC45A3-ELK4 mRNA expression is heterogeneous, highly induced in a subset of prostate cancers, androgen regulated, and most commonly occurs through a mechanism other than chromosomal rearrangement (e.g., trans-splicing).

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • Chromosome Deletion
  • Chromosomes, Human, Pair 1
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • In Situ Hybridization, Fluorescence
  • Male
  • Metribolone / pharmacology
  • Oncogene Proteins, Fusion / biosynthesis
  • Oncogene Proteins, Fusion / genetics*
  • Prostatic Neoplasms / genetics*
  • Prostatic Neoplasms / metabolism
  • Proto-Oncogene Proteins c-ets / biosynthesis
  • Proto-Oncogene Proteins c-ets / genetics
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics*
  • Testosterone Congeners / pharmacology
  • Transcription, Genetic

Substances

  • Oncogene Proteins, Fusion
  • Proto-Oncogene Proteins c-ets
  • RNA, Messenger
  • SLC45A3-ELK4 fusion protein, human
  • Testosterone Congeners
  • Metribolone