Exerts Tumor-Suppressive Functions in Prostate Cancer via Suppression.

The development of novel therapies or the improvement of currently used approaches to treat prostate cancer (PCa), the most frequently diagnosed male tumor in developed countries, is an urgent need. In this regard, the functional characterization of microRNAs, molecules shown to regulate a number of cancer-related pathways, is instrumental to their possible clinical exploitation. Here, we demonstrate the tumor-suppressive role of the so far uncharacterized , which we found to be significantly down-modulated in PCa clinical specimens compared to normal tissues.

Gene expression dataset of prostate cells upon / modulation.

Although the role of 205 has been widely elucidated, the function of its host gene () is yet to be clarified. We have recently investigated whether this gene is a simple endorsement for miRNA production or it may act independently, demonstrating its action as nuclear long noncoding RNA able to control basal-luminal differentiation in the human prostate context, thus deserving the reannotation as , Long Epithelial -interacting Differentiation-related RNA. Here, we describe the loss and gain of function approaches experimentally used to modulate expression, and the bioinformatic procedures employed to analyze microarray data in our published article "LEADeR role of miR-205 host gene as long noncoding RNA in prostate basal cell differentiation" [1].

LEADeR role of miR-205 host gene as long noncoding RNA in prostate basal cell differentiation.

Though miR-205 function has been largely characterized, the nature of its host gene, MIR205HG, is still completely unknown. Here, we show that only lowly expressed alternatively spliced MIR205HG transcripts act as de facto pri-miRNAs, through a process that involves Drosha to prevent unfavorable splicing and directly mediate miR-205 excision. Notably, MIR205HG-specific processed transcripts revealed to be functional per se as nuclear long noncoding RNA capable of regulating differentiation of human prostate basal cells through control of the interferon pathway.