LncRNA TUG 1 knockdown mitigates inflammatory injury induced 1 by cigarette smoke extract in chronic obstructive pulmonary disease 2 via miR-34 c / BRD 4 axis 3 4

17 Chronic obstructive pulmonary disease (COPD) is a type of respiratory disease. The 18 dysregulation of long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) 19 has been reported in diverse diseases. This study aimed to explore the functions and 20 mechanism of TUG1 in COPD. The levels of TUG1 and BRD4 were significantly 21 up-regulated, and the level of miR-34c was apparently down-regulated in COPD 22 D ow naded rom http://pndpress.com /bioscirep/adf/doi/10.1042/BSR 20193896/8/bsr-2019-3896.pdf by gest on 19 Sptem er 2020 Biocience R eorts. This is an Acepted M ancript. ou re encuraged to se he Vrsion of R eord tat, w en puished, w ill relace his vesion. he m st up-tote-version is avilable at https://dg/10.1042/BSR 2093896 patients or CSE-treated BEAS-2B cells. TUG1 was verified to sponge to miR-34c, 23 and BRD4 was validated as a target of miR-34c. TUG1 depletion or miR-34c 24 overexpression promoted cell proliferation but restrained apoptosis, inflammatory 25 response in CSE-treated BEAS-2B cells. MiR-34c inhibitor mitigated the inhibitory 26 effect on cell proliferation and the promotion effects on cell apoptosis, inflammatory 27 response in CSE-treated BEAS-2B cells induced by TUG1 silencing. Mechanistically, 28 TUG1 modulated BRD4 expression in CSE-treated BEAS-2B cells by sponging 29 miR-34c. TUG1 modulated BRD4 to regulate cell proliferation, cell apoptosis and 30 inflammatory response in CSE-treated BEAS-2B cells by sponging miR-34c. 31 32