Abstract
Prostate cancer is a significant health problem around the world. It ranks second in newly diagnosed cancers and sixth in leading causes of cancer death among men. More than half of prostate cancer cases have E twenty-six (ETS) gene fusions, which are potential diagnostic markers for prostate cancer. TMPRSS2: ERG gene fusions are the most common types of gene fusions in prostate cancer. However, the association between TMPRSS2: ERG gene fusions and the aggressiveness of prostate cancer remains elusive. Recent studies showed conflicted results. We hypothesize that some N-terminal truncated ERG proteins encoded by TMPRSS2: ERG fusion genes account for the conflict. Overexpression of full length ERG protein promotes the transcriptional activation of oncogenes and facilitates cancer progression. However some N-terminal truncated ERG proteins might inhibit the oncogenic transcriptional activation by competitive binding to ETS domain binding sites in prostate cancer. And prostate cancers that expressing truncated ERG proteins of these types might possess less aggressive features.
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