ERG oncogene modulates prostaglandin signaling in prostate cancer cells

Ahmed A. Mohamed, Shyh Han Tan, Chen Sun, Syed Shaheduzzaman, Ying Hu, Gyorgy Petrovics, Yongmei Chen, Isabell A. Sesterhenn, Hua Li, Taduru Sreenath, David G. McLeod, Albert Dobi*, Shiv Srivastava

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

31 Scopus citations


Androgen dependent induction of the ETS related gene (ERG) expression in more than half of all prostate cancers results from gene fusions involving regulatory sequence of androgen regulated genes (i.e., TMPRSS2, SLC45A3 and NDRG1) and protein coding sequence of the ERG. Emerging studies in experimental models underscore the functions of ERG in prostate tumorigenesis. However, biological and biochemical functions of ERG in prostate cancer (CaP) remain to be elucidated. This study suggests that ERG activation plays a role in prostaglandin signaling because knockdown of ERG expression in TMPRSS2-ERG fusion containing CaP cells leads to altered levels of the 15-hydroxy- prostaglandin dehydrogenase (HP GD), a tumor suppressor and prostaglandin catabolizing enzyme and prostaglandin E2 (PGE2). We demonstrate that HPGD expression is regulated by the binding of the ERG protein to the core promoter of this gene. Moreover, prostaglandin E2 dependent cell growth and urokinase-type plasminogen activator (uPA ) expression are also affected by ERG knockdown. Together, these data imply that the ERG oncoprotein in CaP cells positively influence prostaglandin mediated signaling, which may contribute to tumor progression.

Original languageEnglish
Pages (from-to)410-417
Number of pages8
JournalCancer Biology and Therapy
Issue number4
StatePublished - 15 Feb 2011
Externally publishedYes


  • Cancer
  • ERG
  • ETS
  • HPGD
  • Inflammation
  • Oncogene
  • Prostaglandin
  • Prostate
  • Tumor suppressor


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