Abstract
Chronic obstructive pulmonary disease (COPD) is a type of respiratory disease. The dysregulation of long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) has been reported in diverse diseases. This study aimed to explore the functions and mechanism of TUG1 in COPD. The levels of TUG1 and BRD4 were significantly up-regulated, and the level of miR-34c was apparently down-regulated in COPD patients or CSE-treated BEAS-2B cells. TUG1 was verified to sponge to miR-34c, and BRD4 was validated as a target of miR-34c. TUG1 depletion or miR-34c overexpression promoted cell proliferation but restrained apoptosis, inflammatory response in CSE-treated BEAS-2B cells. MiR-34c inhibitor mitigated the inhibitory effect on cell proliferation and the promotion effects on cell apoptosis, inflammatory response in CSE-treated BEAS-2B cells induced by TUG1 silencing. Mechanistically, TUG1 modulated BRD4 expression in CSE-treated BEAS-2B cells by sponging miR-34c. TUG1 modulated BRD4 to regulate cell proliferation, cell apoptosis and inflammatory response in CSE-treated BEAS-2B cells by sponging miR-34c.
Highlights
WITHDRAWN: LncRNA TUG1 knockdown mitigates inflammatory injury induced by cigarette smoke extract in chronic obstructive pulmonary disease via miR-34c/BRD4 axis
The Accepted Manuscript version of this article (published on 19 August 2020) was withdrawn on 3 December 2020 due to concerns over data validity
Summary
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