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In the United States, prostate cancer is the second leading cause of cancer-related deaths among men with an approximately 220,000 patients diagnosed with the disease in 2015. Prostate cancer is a hormone-driven tumor, and a common therapy is androgen-deprivation therapy (ADT) that involves anti-androgen treatments and/or castration therapy. Understanding the molecular basis for androgen-independent tumors is crucial toward developing new therapies for these patients. Understanding how androgen receptor itself functions is an important step in elucidating this process. Androgen receptor (AR), NR3C4, is a nuclear hormone receptor and functions as a DNA-binding transcription factor that regulates the expression of protein-coding genes. Translocation of AR to improper gene promoter elements or DNA-binding sites can result in an alteration in gene expression and thus normal prostate function. Therefore, it is crucial to understand which AR-promoter interactions are drivers of disease, as compared to promiscuous or benign AR-binding interactions. While a large portion of our genome is considered a gene desert, it is now appreciated that these regions of the genome contain non-coding RNA genes such as microRNAs (miRNAs). These non-coding RNAs have enormous regulatory potential, as they post-transcriptionally regulate gene expression by binding to messenger RNAs (mRNAs) to promote degradation or intervention of translational processes. In this review, we focus specifically on the notion that mis-regulation of non-coding RNAs such as miRNAs by improper AR–DNA binding are an important component that promotes prostate cancer. We also highlight the role of miR-206 and the interaction of miR-206 and AR within this process, given this is a miRNA known to be regulated by hormones in both breast and prostate cancer. [ABSTRACT FROM PUBLISHER]

Triple negative breast cancer (TNBC) has been associated with the lack of three hormone receptors; estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER-2). However, a host of other steroid hormone receptors such as vitamin D receptor (VDR) is present in TNBC, and the role of these hormone receptors in breast tumorigenesis is unclear. The levels of microRNAs (miRNAs) are also expressed differently than in normal mammary epithelial cells. miRNAs are regulatory RNAs involved in various cellular functions, mainly gene silencing. Here, we reviewed the literature surrounding miRNAs in breast cancer, and performedin silicoanalysis to determine whether there was a correlation between levels of VDR in relation to miRNAs important in breast cancer development and tumorigenesis. We identified three miRNAs of interest, specifically, miR-23, miR-124, and miR-125. Through this research we determined the possibility that these miRNAs play an important role in controlling VDR activity and by virtue the development of breast cancer. [ABSTRACT FROM AUTHOR]