The oncogenic transcription factor ERG represses the transcription of the tumour suppressor gene PTEN in prostate cancer cells | Zendy

Patricia Adamo | Zendy; Sean Porazinski | Zendy; Shavanthi Rajatileka | Zendy; Samantha L. Jumbe | Zendy; R Hagen | Zendy; ManKim Cheung | Zendy; Ian Wilson | Zendy; Michael Ladomery | Zendy

Open Access

The oncogenic transcription factor ERG represses the transcription of the tumour suppressor gene PTEN in prostate cancer cells

Author(s) -

Patricia Adamo,

Sean Porazinski,

Shavanthi Rajatileka,

Samantha L. Jumbe,

R Hagen,

ManKim Cheung,

Ian Wilson,

Michael Ladomery

Publication year - 2017

Publication title -

oncology letters

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.766

H-Index - 54

eISSN - 1792-1082

pISSN - 1792-1074

DOI - 10.3892/ol.2017.6841

Subject(s) - pten , cancer research , tensin , biology , prostate cancer , oncogene , transcription factor , tumor suppressor gene , erg , carcinogenesis , cancer , pi3k/akt/mtor pathway , gene , microbiology and biotechnology , cell cycle , genetics , signal transduction , retina , neuroscience

The oncogene ETS-related gene (ERG) encodes a transcription factor with roles in the regulation of haematopoiesis, angiogenesis, vasculogenesis, inflammation, migration and invasion. The ERG oncogene is activated in >50% of prostate cancer cases, generally through a gene fusion with the androgen-responsive promoter of transmembrane protease serine 2. Phosphatase and tensin homologue ( PTEN ) is an important tumour suppressor gene that is often inactivated in cancer. ERG overexpression combined with PTEN inactivation or loss is often associated with aggressive prostate cancer. The present study aimed to determine whether or not ERG regulates PTEN transcription directly. ERG was demonstrated to bind to the PTEN promoter and repress its transcription. ERG overexpression reduced endogenous PTEN expression, whereas ERG knockdown increased PTEN expression. The ability of ERG to repress PTEN may contribute to a more cancer-permissive environment.

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