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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.
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Zhao et al. (2016) studied this question.
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