Quantitative expression of TMPRSS2 transcript in prostate tumor cells reflects TMPRSS2-ERG fusion status

K. Mwamukonda, Y. Chen, L. Ravindranath, B. Furusato, Y. Hu, J. Sterbis, D. Osborn, I. Rosner, I. A. Sesterhenn, D. G. McLeod, S. Srivastava, G. Petrovics*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


TMPRSS2-ERG fusion is the most common oncogenic rearrangement in prostate cancer (CaP). Owing to this chromosomal rearrangement one TMPRSS2 allele loses its promoter, and one of the ETS-related gene (ERG) alleles gains that promoter leading to its overexpression in these tumor cells. Some studies suggest that TMPRSS2, an androgen-regulated type II transmembrane serine protease, may have an effect on CaP progression. We hypothesized that a difference in TMPRSS2 expression may be present in vivo between CaP cells with and without TMPRSS2-ERG fusion, or a compensatory mechanism for the allelic loss of TMPRSS2 may balance that expression difference. Therefore, TMPRSS2 mRNA expression was evaluated in microdissected CaP cells with and without TMPRSS2-ERG fusion in 132 CaP patients and analyzed for its correlation with other androgen receptor (AR)-regulated genes and clinicopathological features. In vivo TMPRSS2 expression correlated with that of other AR-regulated genes, including PSA/KLK3 and PMEPA1, offering potential as AR surrogates. A significantly reduced expression of TMPRSS2 was evident in malignant cells harboring TMPRSS2-ERG fusion, but not in CaP cells without TMPRSS2-ERG fusion, further defining these two genetically distinct types of CaP.

Original languageEnglish
Pages (from-to)47-51
Number of pages5
JournalProstate Cancer and Prostatic Diseases
Issue number1
StatePublished - Mar 2010
Externally publishedYes


  • Quantitative expression
  • TMPRSS2-ERG fusion


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