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Deletion of Interstitial Genes between TMPRSS2 and ERG Promotes Prostate Cancer Progression

Douglas E Linn1, Kathryn L Penney2, Roderick T Bronson3

  • 1Division of Genetics, Brigham and Women's Hospital and Department of Medicine, Harvard Medical School, Boston, Massachusetts.

Cancer Research
|February 17, 2016
PubMed

Insights

Loss of genes in the TMPRSS2-ERG interstitial region, including Ets2, drives aggressive prostate cancer. This deletion promotes tumor progression and poor differentiation in PTEN-deficient mice, highlighting Ets2 as a tumor suppressor.

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • TMPRSS2-ERG gene fusions are common in prostate cancer, arising from chromosomal rearrangements or deletions.
  • Intrachromosomal deletion removes a ~3-Mb interstitial region with largely unexplored genes relevant to prostate cancer.

Purpose of the Study:

  • To investigate the role of the interstitial region deleted during TMPRSS2-ERG fusion formation in prostate cancer development.
  • To characterize mouse models mimicking TMPRSS2-ERG insertion or deletion in PTEN-deficient prostates.

Main Methods:

  • Development and analysis of two distinct mouse models for TMPRSS2-ERG rearrangement.
  • Prostate-specific PTEN deficiency was introduced into the mouse models.
  • Gene expression analysis and mechanistic investigations of interstitial genes, including Ets2 and Bace2.

Main Results:

  • Mice lacking the interstitial region developed aggressive prostate adenocarcinomas with poor differentiation and epithelial-to-mesenchymal transition.
  • Reduced expression of interstitial genes Ets2 and Bace2 correlated with biochemical relapse and lethal disease in human prostate cancer.
  • Knockout of Ets2 in PTEN-deficient mice accelerated prostate adenocarcinoma progression, partly via MAPK signaling activation.

Conclusions:

  • The deleted interstitial region contains tumor suppressor genes critical for prostate cancer progression.
  • Ets2 functions as a tumor suppressor in prostate cancer, and its loss contributes to disease aggressiveness.
  • Loss of Ets2 and other interstitial genes promotes prostate cancer development and progression.

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