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Retracted : Negative feedback of NF‐κB signaling by long noncoding RNA MALAT1 controls lipopolysaccharide‐induced inflammation injury in human lung fibroblasts WI‐38
Author(s) -
Zhu Wei,
Men Xuelin
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29429
Subject(s) - malat1 , inflammation , lipopolysaccharide , apoptosis , nf κb , cancer research , signal transduction , cytokine , long non coding rna , biology , downregulation and upregulation , immunology , microbiology and biotechnology , gene , biochemistry
The study was designed to elucidate the regulatory mechanism of long noncoding RNA human metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in lipopolysaccharides (LPS)‐caused inflammation injury in human lung fibroblasts WI‐38. WI‐38 cells were stimulated with LPS to construct acute pneumonia cell model. MALAT1 in LPS‐stimulated WI‐38 cells was examined. LPS‐induced inflammation injury was estimated using viability, apoptosis, and cytokine secretion including interleukin‐1β (IL‐1β) and IL‐6. Furthermore, the modulatory relations of MALAT1 and nuclear factor‐kappa B (NF‐κB) signaling were explored. We found that the sensitivity of WI‐38 cells to apoptosis was enhanced by LPS‐caused inflammation. Moreover, LPS promoted MALAT1 expression which was found to alleviate LPS‐caused damages. Besides, NF‐κB p65 overexpression resulted in an increased expression of MALAT1, and MALAT1 was identified as a target gene of p65. Furthermore, overexpression of MALAT1 reduced NF‐κB activation. Pulldown assay showed that MALAT1 could directly interact with p65. Taken together, our findings revealed that MALAT1 was upregulated in LPS‐stimulated WI‐38 cells. Through directly interacting with p65, MALAT1 blocked LPS‐caused activation of NF‐κB and repressed LPS‐induced inflammation injury. MALAT1 may serve as a potential diagnostic indicator or therapeutic target for pneumonia.