Abstract
Prostate cancer is a gland tumor in the male reproductive system. It is a multifaceted and genomically complex disease. Transmembrane protease, serine 2 and v-ets erythroblastosis virus E26 homolog (TMPRSS2-ERG) gene fusions are the common molecular signature of prostate cancer. Although tremendous advances have been made in unraveling various facets of TMPRSS2-ERG-positive prostate cancer, many research findings must be sequentially collected and re-interpreted. It is important to understand the activation or repression of target genes and proteins in response to various stimuli and the assembly in signal transduction in TMPRSS2-ERG fusion-positive prostate cancer cells. Accordingly, we divide this multi-component review ofprostate cancer cells into several segments: 1) The role of TMPRSS2-ERG fusion in genomic instability and methylated regulation in prostate cancer and normal cells; 2) Signal transduction cascades in TMPRSS2-ERG fusion-positive prostate cancer; 3) Overexpressed genes in TMPRSS2-ERG fusion-positive prostate cancer cells; 4) miRNA mediated regulation of the androgen receptor (AR) and its associated protein network; 5) Quantitative control of ERG in prostate cancer cells; 6) TMPRSS2-ERG encoded protein targeting; In conclusion, we provide a detailed understanding of TMPRSS2-ERG fusion related information in prostate cancer development to provide a rationale for exploring TMPRSS2-ERG fusion-mediated molecular network machinery.
Highlights
Multiple molecular signaling pathways overlap, integrate and promote the progression of intraepithelial neoplasia and metastasis
Cysteine-rich secretory protein 3 (CRISP3) gene expression was found to be associated with the ERG condition, since it was overexpressed in TMPRSS2-ERG fusion-positive prostate tumors as compared to normal tissue
Genomic rearrangement has added another layer of complexity to prostate cancer investigation and has been emerged as major challenge to targeted therapeutic research
Summary
Multiple molecular signaling pathways overlap, integrate and promote the progression of intraepithelial neoplasia and metastasis. We will briefly discuss difference of TMPRSS2-ERG positive and negative prostate cancer cells and how gene networks are regulated in fusion positive cancer cells. The expression of transcription factor ERG may be regulated through the promoter of the androgen-responsive gene TMPRSS2.
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