Nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway (NF-κB) and microRNA-mediated regulation (NF-κB pathway (for the pathway); miRNA (for microRNA-mediated regulation))

This entry describes the *crosstalk* between the **NF-κB signaling pathway**—a master regulator of inflammation, immune responses, cell proliferation, and survival—and **microRNAs (miRNAs)**, small non-coding RNAs that modulate gene expression post-transcriptionally. NF-κB not only regulates genes encoding inflammatory mediators and survival factors but also induces (and is regulated by) a variety of miRNAs, forming intricate feedback and feedforward loops. Examples include miR-155 (amplifies NF-κB activity and inflammation in macrophages) and miR-146a (negatively regulates NF-κB, promoting resolution of inflammation)[1][3][4][7]. In cancer, chronic inflammation, and autoimmune diseases, this complex network can become dysregulated, contributing to disease pathogenesis and progression. While individual components (e.g., NF-κB subunits, certain miRNAs) are considered drug targets, the network as a whole is not a singular, targetable molecule but a multi-module regulatory system[1][3][6].

Other names

NF-κB signaling and miRNA regulatory networkNF-κB–microRNA feedback loopNF-κB and miRNA crosstalk

Inhibit NF-κB activation (proteasome inhibition, IKK inhibition). Modulate miRNA expression or function (e.g., antagomirs, miRNA mimics; experimental). Block signal transduction upstream (e.g., TLR4 antagonism impacts NF-κB activation).