Journal
CLINICAL AND TRANSLATIONAL MEDICINE
Volume 11, Issue 7, Pages -Publisher
JOHN WILEY & SONS LTD
DOI: 10.1002/ctm2.479
Keywords
chronic obstructive pulmonary disease; early B-cell factor 1; hsa-miR-149-5p; IL-6; IL6-AS1; inflammation; long noncoding RNA
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Funding
- National Natural Science Foundation of China [81970045, 81670040]
- Local Innovative and Research Teams Project of Guangdong Pearl River Talents Program [2017BT01S155]
- Guangdong Province Key Field RD Program [2020B1111330001]
- National Key Research and Development Program [2016YFC1304101]
- Characteristic Innovation Projects of Universities in Guangdong Province [2019KTSCX139]
- Zhongnanshan Medical Foundation of Guangdong Province [ZNSA-2020003]
- Nanshan Medical Development Foundation of Guangdong Province
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IL6-AS1 is upregulated in chronic obstructive pulmonary disease and promotes inflammation by enhancing the expression of inflammatory factors. It acts as an endogenous sponge in the cytoplasm to stabilize IL-6 mRNA, and in the nucleus, it recruits early B-cell factor 1 to promote IL-6 transcription.
Chronic obstructive pulmonary disease is a complex condition with multiple etiologies, including inflammation. We identified a novel long noncoding RNA (lncRNA), interleukin 6 antisense RNA 1 (IL6-AS1), which is upregulated in this disease and is associated with airway inflammation. We found that IL6-AS1 promotes the expression of inflammatory factors, especially interleukin (IL) 6. Mechanistically, cytoplasmic IL6-AS1 acts as an endogenous sponge by competitively binding to the microRNA miR-149-5p to stabilize IL-6 mRNA. Nuclear IL6-AS1 promotes IL-6 transcription by recruiting early B-cell factor 1 to the IL-6 promoter, which increases the methylation of the H3K4 histone and acetylation of the H3K27 histone. We propose a model of lncRNA expression in both the nucleus and cytoplasm that exerts similar effects through differing mechanisms, and IL6-AS1 probably increases inflammation via multiple pathways.
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