| Literature DB >> 27861797 |
Yu Wang1, Xiaoyu Chen2, Guodong Tang2, Dingyang Liu2, Gang Peng2, Wenbin Ma1, Qing Liu2,3, Jian Yuan2,3.
Abstract
Interleukin-6 (IL-6) is widely expressed in a variety of malignant tumors; thus, targeting the IL-6/STAT3 pathway represents a promising therapeutic strategy for malignant cancers. In this study, we identified a noncoding RNA, AS-IL6, which is transcribed antisense to IL6 and induces IL6 expression in glioma cells. Knockdown of AS-IL6 attenuates LPS-induced IL6 transcription. Interestingly, AS-IL6 does not change IL6 mRNA stability, but induces the enrichment of histone H3 acetylated at lysine 27 (H3K27Ac) at the IL6 promoter. In addition, we found that depletion of AS-IL6 inhibits the invasive ability of glioblastoma cells, while treatment of cells with recombinant IL6 reverses this effect. Our results reveal a novel mechanism of IL6 regulation and demonstrate an oncogenic role for AS-IL6 in glioma cells.Entities:
Keywords: zzm321990AS-IL6zzm321990; H3K27Ac; STAT3; cell invasion; interleukin-6
Mesh:
Substances:
Year: 2016 PMID: 27861797 DOI: 10.1002/1873-3468.12485
Source DB: PubMed Journal: FEBS Lett ISSN: 0014-5793 Impact factor: 4.124