miR-183 potentially inhibits NF-κB1 expression by directly targeting its 3′-untranslated region

Abstract

Nuclear factor-kB (NF-kB) is an important transcription factor. While the NF-kB signaling pathway is modulated by many microRNAs (miRNAs), very few have been reported to target NF-kB1 gene directly. In this study, we used multiple miRNA target prediction programs to predict miRNAs with putative NF-kB1 3 0 -untranslated region (UTR) binding sites. miR-183 was strongly implicated and experimentally validated by reporter assays. The results showed a reduced expression of the NF-kB1 3 0 UTR containing luciferase vector by ∼30%, which was comparable to the reduction by miR-9 (the only known miRNA targeting the NF-kB1 3 0 UTR). Mutagenesis of the miR-183 seed region binding sequence in the NF-kB1 3 0 UTR abolished the inhibitory effect of miR-183, as noted by the NF-kB1 3 0 UTRcontaining reporter. Moreover, similar to miR-9, miR-183 could down-regulate the expression of the reporter driven by NF-kB promoter to some degree, suggesting that miR-183 might negatively regulate the endogenous NF-kB1. Overall, our data provide computational and experimental evidence that NF-kB1 is a potential target of miR-183.

Effects of hypercapnia on the lung

“…A recent report demonstrated that miR‐183 inhibits NF‐κB by directly targeting its 3′‐untranslated region (Sha et al . ). In addition, miR‐183 is known to negatively regulate cell migration in cancer cells (Lowery et al .…”

microRNA‐183 improve myocardial damager via NF‐kb pathway: In vitro and in vivo study

“…Extensive studies have demonstrated that miRNA can effectively alleviate myocardial injury induced by myocardial I/R through direct or indirect anti‐inflammatory mechanisms . NF‐κb has an important role in inflammatory mechanisms, meanwhile, some previous studies reported NF‐κb was an target gene of miRNA‐183 . We inferred that miRNA‐183 overexpression may have effects to improve myocardial damager through NF‐kb pathway.…”

“…[13][14][15] NF-κb has an important role in inflammatory mechanisms, meanwhile, some previous studies reported NF-κb was an target gene of miRNA-183. 9,10 We inferred that miRNA-183 overexpression may have effects to improve myocardial damager through NF-kb pathway.…”

“…8 Meanwhile, some previous studies explained that NF-κB was the target of microRNA-183 (miRNA-183). 9,10 However, it has been unclear that the effects and mechanism of miRNA-183 in I/R induced myocardial damager. In our present study, we explain that miRNA-183 has effects to improve I/R induced myocardial damager by vitro and in vivo studies.…”

The enhancer activity of long interspersed nuclear element derived microRNA 625 induced by NF-κB

“…miRNA and NF-κB studies revealed the NF-κB-miRNA network, which provides a better understanding of the regulation and cooperation of inflammation and cancer in various cancer types [35][36][37] . In addition to inducing expression, miRNAs repress NF-κB by direct targeting 38 .…”