Abstract
The androgen receptor (AR) is a member of the steroid hormone receptor family of nuclear transcription factors. It is present in the primary/secondary sexual organs, kidneys, skeletal muscles, adrenal glands, skin, nervous system, and breast. Abnormal AR functioning has been identified in numerous diseases, specifically in prostate cancer (PCa). Interestingly, recent studies have indicated a relationship between the AR and microRNA (miRNA) crosstalk and cancer progression. MiRNAs are small, endogenous, non-coding molecules that are involved in crucial cellular processes, such as proliferation, apoptosis, or differentiation. On the one hand, AR may be responsible for the downregulation or upregulation of specific miRNA, while on the other hand, AR is often a target of miRNAs due to their regulatory function on AR gene expression. A deeper understanding of the AR–miRNA interactions may contribute to the development of better diagnostic tools as well as to providing new therapeutic approaches. While most studies usually focus on the role of miRNAs and AR in PCa, in this review, we go beyond PCa and provide insight into the most recent discoveries about the interplay between AR and miRNAs, as well as about other AR-associated and AR-independent diseases.
Highlights
The androgen receptor (AR), together with the estrogen, progesterone, and glucocorticoid receptors, belongs to the steroid hormone receptor family, which acts as a liganddependent transcription factor
The circulating androgens bind to the androgen receptor that is located in the cytoplasm, which is associated with heat shock proteins (HSP) and other chaperons, which, in turn, initiates the transport of the AR dimers to the nucleus
It is possible that AR promotes the progression of this type of cancer through controlling the expression of miRNAs that are crucial for breast cancers (BC) development, such as miR-125b, miR-21, and let-7a
Summary
The androgen receptor (AR), together with the estrogen, progesterone, and glucocorticoid receptors, belongs to the steroid hormone receptor family, which acts as a liganddependent transcription factor. MiRNAs are small (about 17–25 nucleotides in length), non-coding, single-stranded, endogenous molecules that play an important role in the regulation of post-transcriptional gene expression by interacting with the 30 untranslated region (30 UTR) of its target messenger RNA (mRNA) [9,10]. One of the strands of miRNA is removed, and another is bound to the AGO2 protein, which is a member of RISC (RNA-included silencing complex) This complex can target the 30 UTR region of the mRNA, which results in mRNA deadenylation, translational repression, or mRNA cleavage [25,27,28]. In PCa cells, AR associates with KDM1A (lysine-specific demethylase 1), which enables the removal of repressive methyl marks in AR-targeted genes [37] This modulates the methylation of the promoter elements of AR-upregulated miRNAs (miR-22 and miR-29a) [38]. AR is a target for miR-124a; miR-124a determines the expression of AR gene in human thyroid cancer tissues [65]
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