The long noncoding RNA MALAT1 regulates the lipopolysaccharide-induced inflammatory response through its interaction with NF-κB

Abstract

MALAT1 is a conserved long noncoding RNA whose expression correlates with many human cancers. However, its significance in immunity remains largely unknown. Here, we observe that MALAT1 is upregulated in lipopolysaccharide (LPS)-activated macrophages. Knockdown of MALAT1 increases LPS-induced expression of TNFα and IL-6. Mechanistically, MALAT1 was found to interact with NF-κB in the nucleus, thus inhibiting its DNA binding activity and consequently decreasing the production of inflammatory cytokines. Additionally, abnormal expression of MALAT1 was found to be NF-κB-dependent. These findings suggest that MALAT1 may function as an autonegative feedback regulator of NF-κB to help fine-tune innate immune responses.

Keywords: MALAT1; Macrophage; NF-κB transcription factor; inflammation; innate immunity.