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AS ‐ IL 6 promotes glioma cell invasion by inducing H3K27Ac enrichment at the IL 6 promoter and activating IL 6 transcription
Author(s) -
Wang Yu,
Chen Xiaoyu,
Tang Guodong,
Liu Dingyang,
Peng Gang,
Ma Wenbin,
Liu Qing,
Yuan Jian
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 - 10.1002/1873-3468.12485
Subject(s) - gene knockdown , glioma , interleukin 6 , transcription (linguistics) , cancer research , promoter , biology , stat3 , microbiology and biotechnology , transcription factor , chemistry , cell culture , cytokine , gene expression , gene , signal transduction , immunology , genetics , linguistics , philosophy
Interleukin‐6 ( IL ‐6) is widely expressed in a variety of malignant tumors; thus, targeting the IL‐6/ STAT 3 pathway represents a promising therapeutic strategy for malignant cancers. In this study, we identified a noncoding RNA , AS ‐ IL 6 , which is transcribed antisense to IL 6 and induces IL 6 expression in glioma cells. Knockdown of AS ‐ IL 6 attenuates LPS ‐induced IL 6 transcription. Interestingly, AS ‐ IL 6 does not change IL 6 mRNA stability, but induces the enrichment of histone H3 acetylated at lysine 27 (H3K27Ac) at the IL 6 promoter. In addition, we found that depletion of AS ‐ IL 6 inhibits the invasive ability of glioblastoma cells, while treatment of cells with recombinant IL 6 reverses this effect. Our results reveal a novel mechanism of IL 6 regulation and demonstrate an oncogenic role for AS ‐ IL 6 in glioma cells.
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