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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. At molecular level,  MIR205HG  directly binds the promoters of its target genes, which have an  Alu  element in proximity of the Interferon-Regulatory Factor (IRF) binding site, and represses their transcription likely buffering IRF1 activity, with the ultimate effect of preventing luminal differentiation. As  MIR205HG  functions autonomously from (albeit complementing)  miR-205  in preserving the basal identity of prostate epithelial cells, it warrants reannotation as  LEADeR  (Long Epithelial  Alu -interacting Differentiation-related RNA).

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