Mir-141 regulates proliferation and apoptosis of lung fibroblasts by targeting ZEB1

• Main Authors: Yi-Xiu Yang, Yi-Peng Ding
• Format: Article
• Language: English
• Published: Editorial Board of Journal of Hainan Medical University 2020-11-01
• Series: Journal of Hainan Medical University
• Subjects: copd; mir-141; zeb1; proliferation; apoptosis
• Online Access: http://www.hnykdxxb.com/PDF/201922/03.pdf

Objective: To study the significance of mir-141 expression in COPD (chronic obstructive pulmonary diseases) mononuclear cells, and to demonstrate its effect on proliferation and apoptosis of fibroblasts Possible to ZEB1(zinc finger E-box binding homeobox 1). Methods: 40 cases acute phase of COPD patients, 80 cases of stable period COPD patients and 110 normal controls in our hospital were collected. RT-PCR was used to detect mir-141 and statistical analysis. The mir-141 mimic was constructed and transfected into lung fibroblasts. The expression of mir-141 was analyzed by RT-PCR. Cell proliferation was analyzed by CCK8 and cell apoptosis was detected by flow cytometry. Targetscan was used to predict the binding site of ZEB1 and mir-141. The target relationship between ZEB1 and mir-141 was identified by RT-PCR and western blot. Results: The expression of mir-141 in mononuclear cells of acute phase of COPD and stable period of COPD was significantly higher than that of normal controls. Mir-141 levels in acute phase of COPD were significantly higher than that of stable period of COPD. Mir-141 mimic transfection significantly up-regulated the expression of mir- 141, promoted cell activity and decreased cell apoptosis rate compared with the empty control group. ZEB1 and mir-141 had binding sites predicted by Targetscan database and verified by dual luciferase assays. After mir-141 mimic transfection hat, ZEB1 mRNA and protein expression were down-regulated. Conclusions: High expression of mir-141 in COPD may promote the proliferation of lung fibroblasts and inhibit apoptosis by targeting ZEB1.