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Background  MicroRNA-155 (miR-155) is the diced product of the  MIR155HG  gene. miR-155 regulates the expression of many immune-specific transcripts, is overexpressed in many human lymphomas, and has oncogenic activity in mouse transgenic models.  MIR155HG  has been proposed to be a target gene for transcription factor NF-κB largely due to the positive correlation between high nuclear NF-κB activity and increased miR-155 expression following treatment with NF-κB inducers or in subsets of hematopoietic cancers. Nevertheless, direct regulation of the human  MIR155HG  promoter by NF-κB has not been convincingly demonstrated previously.    Results  This report shows that induction of NF-κB activity rapidly leads to increased levels of both primary  MIR155HG  mRNA and mature miR-155 transcripts. We have mapped an NF-κB-responsive element to a position approximately 178 nt upstream of the  MIR155HG  transcription start site. The -178 site is specifically bound by the NF-κB p50/p65 heterodimer and is required for p65-induced reporter gene activation. Moreover, the levels of miR-155 in nine human B-lymphoma cell lines generally correlate with increased nuclear NF-κB proteins.    Conclusion  Overall, the identification of an NF-κB-responsive site in the  MIR155HG  proximal promoter suggests that  MIR155HG  is a direct NF-κB target gene  in vivo . Understanding NF-κB-mediated regulation of miR-155 could lead to improved immune cell-related diagnostic tools and targeted therapies.

Identification of an NF-κB p50/p65-responsive site in the human MIR155HG promoter