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Retracted : HOTAIR regulates lipopolysaccharide‐induced inflammatory response in hepatocytes
Author(s) -
Zhang Jianhua,
Chen Miao,
Zhai Yuyan,
Fu Yu
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29301
Subject(s) - hotair , gene knockdown , small interfering rna , biology , cancer research , janus kinase , tumor necrosis factor alpha , microbiology and biotechnology , cell culture , signal transduction , long non coding rna , downregulation and upregulation , transfection , immunology , biochemistry , genetics , gene
It has been widely accepted that long‐noncoding RNA (lncRNA) HOX transcript antisense intergenic RNA (HOTAIR) emerges as a crucial mediator in inflammation. Here, we first detected HOTAIR in lipopolysaccharide (LPS)‐treated normal human liver cell line (L02) and hepatocellular carcinoma cell lines (C3A, HepG2, and SMMC‐7721). Further, we explored the biological function of HOTAIR in LPS‐induced hepatocytes (L02 and C3A) lesions and investigated the molecular mechanisms. Besides, we focused on inflammatory signaling crosstalk. The inflammatory insults were assayed by cell counting kit‐8 (CCK‐8), cell cycle and apoptosis analysis kit, and immunoblotting assay. HOTAIR level was examined by reverse‐transcription polymerase chain reaction. To determine the effect of HOTAIR silence or overexpression in inflammation, we applied quantitative reverse‐transcription polymerase chain reaction, immunoblotting assay, and enzyme‐linked immuno sorbent assay. Regulator inhibitors of Janus kinase/signal transducer and activator of transcription (JAK2/STAT3; AG490) and nuclear factor κB (NF‐κB; BAY‐11–7082) were applied to treat cells. Our results suggested that LPS induced the overexpression of HOTAIR in L02, C3A, HepG2, and SMMC‐7721 cells. LPS repressed viability, induced apoptosis, and facilitated the expression of interleukin (IL)‐1β, IL‐6, and tumor necrosis factor (TNF)‐α in L02 and C3A cells. IL‐1β, IL‐6, and TNF‐α were upregulated by HOTAIR overexpression while downregulated by HOTAIR knockdown in LPS‐treated cells. We further observed that HOTAIR overexpression accelerated LPS‐induced phosphorylation whereas HOTAIR silence blocked this progress. Inhibition of JAK/STAT and NF‐κB contributed to the suppression of cytokines which was evoked by LPS. Collectively, our findings indicated that HOTAIR exerted a crucial role in cytokines expression by activating JAK/STAT and NF‐κB.