NF-kappaB interacting long non-coding RNA (NKILA)

NF-kappaB interacting long non-coding RNA (NKILA) is a cytoplasmic long non-coding RNA that regulates inflammatory and cancer-related pathways by interacting with the NF-κB/IκB complex, inhibiting phosphorylation of IκB, and thereby preventing NF-κB activation and nuclear translocation. NKILA acts as a tumor suppressor in several cancer types, suppressing proliferation, angiogenesis, and metastasis by downregulating key downstream transcriptional targets and mediating epithelial-mesenchymal transition (EMT). NKILA also negatively regulates HIV-1 replication by repressing NF-κB-dependent viral transcription and can act as a host restriction factor for HIV-1 latency and reactivation. Its expression level is a clinically valuable biomarker for prognosis in various cancers; decreased NKILA is associated with more aggressive disease and worse outcomes. There are currently no approved drugs directly targeting NKILA, but its pathway involvement indicates therapeutic potential in inflammation, cancer, and viral infection.

Other names

NF-κB interacting lncRNANuclear factor NF-κB interacting lncRNANF-kappaB interacting long noncoding RNA

Masks IκB phosphorylation motifs to stabilize the NF-κB/IκB complex, inhibiting IκB phosphorylation and NF-κB activation; Inhibits NF-κB-dependent transcription, impeding processes such as proliferation, metastasis, and inflammation; Suppresses transcriptional initiation of HIV-1 and inhibits viral replication by interfering with recruitment of p65 (NF-κB), NFAT, and SP1 at the HIV-1 LTR; Downregulates target genes involved in EMT (epithelial-mesenchymal transition), e.g., TWIST1, MMP9, CCND1