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Protocols for Studies on TMPRSS2/ERG in Prostate Cancer

Hubert Pakula1, Douglas E Linn1, Daniel R Schmidt2

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

Methods in Molecular Biology (Clifton, N.J.)
|May 23, 2018
PubMed

Insights

TMPRSS2/ERG gene fusions are common in prostate cancer, driving early tumor development. These fusions also reveal ETS2 as a prostate tumor suppressor, crucial for cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • TMPRSS2/ERG gene fusions are the most frequent genetic alterations in human prostate cancer.
  • These fusions result in the aberrant expression of ERG (ETS family transcription factor) in prostate cells.
  • Approximately 60% of these fusions arise from intrachromosomal deletions between TMPRSS2 and ERG.

Purpose of the Study:

  • To create and utilize TMPRSS2/ERG knockin mouse models to study their role in prostate cancer.
  • To investigate the early events in prostate tumorigenesis driven by TMPRSS2/ERG.
  • To identify potential tumor suppressors within the TMPRSS2-ERG interstitial region.

Main Methods:

  • Generation of TMPRSS2/ERG knockin mouse models.
  • In vivo and in vitro studies to analyze prostate cancer development.
  • Analysis of gene expression and tumor suppressor roles.

Main Results:

  • TMPRSS2/ERG acts as an early oncogenic event, sensitizing prostate cells to cooperate with other oncogenic events like PTEN deficiency.
  • The interstitial region between TMPRSS2 and ERG contains ETS2, a prostate tumor suppressor.
  • Loss of ETS2 contributes to prostate cancer progression.

Conclusions:

  • TMPRSS2/ERG knockin mouse models are valuable tools for studying prostate cancer.
  • TMPRSS2/ERG is an early driver of prostate cancer, and ETS2 loss contributes to its progression.
Keywords:
ERGFACSGene fusionInterstitial deletionMouse modelOrganoid culturePTENPb-CreProstate regenerationTMPRSS2

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