WITHDRAWN: LncRNA TUG1 knockdown mitigates inflammatory injury induced by cigarette smoke extract in chronic obstructive pulmonary disease via miR-34c/BRD4 axis

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.

CircANKRD11 Knockdown Protects HPMECs from Cigarette Smoke Extract-Induced Injury by Regulating miR-145-5p/BRD4 Axis

“… 38 Additionally, BRD4 was also found to regulate CSE-triggered cell proliferation, apoptosis and inflammatory response in BEAS-2B cells. 39 In this paper, data also presented that BRD4 was augmented in the lung tissues of smokers with or without COPD as well as CSE-treated HPMECs, and that BRD4 induced cell apoptosis as well as promoted inflammation and oxidative stress, which were in line with the study of Song et al 20 In the meantime, the repressive impacts of BRD4 overexpression on miR-145-5p-mediated action implied that miR-145-5p regulated CSE-induced cell injury by targeting BRD4. Further, rescue experiments displayed that circANKRD11 regulated BRD4 expression by binding to miR-145-5p.…”