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The long noncoding RNA MALAT 1 regulates the lipopolysaccharide‐induced inflammatory response through its interaction with NF ‐κB
Author(s) -
Zhao Gui,
Su Zhenyi,
Song Dan,
Mao Yimin,
Mao Xiaohua
Publication year - 2016
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12315
Subject(s) - malat1 , gene knockdown , innate immune system , lipopolysaccharide , nf κb , downregulation and upregulation , rna , long non coding rna , microbiology and biotechnology , biology , immune system , proinflammatory cytokine , tumor necrosis factor alpha , function (biology) , inflammation , chemistry , immunology , gene , biochemistry , signal transduction
MALAT 1 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 MALAT 1 is upregulated in lipopolysaccharide ( LPS )‐activated macrophages. Knockdown of MALAT 1 increases LPS ‐induced expression of TNF α and IL ‐6. Mechanistically, MALAT 1 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 MALAT 1 was found to be NF ‐κB‐dependent. These findings suggest that MALAT 1 may function as an autonegative feedback regulator of NF ‐κB to help fine‐tune innate immune responses.