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LncRNA RP11-521C20.3 Inhibits Cigarette Smoke Extract-Induced Apoptosis in A549 Cells by Targeting BMF Signaling

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机构： [1]Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, People’s

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关键词： chronic obstructive pulmonary disease lncRNA RP11-521C20 3 BMF apoptosis

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LncRNAs are closely correlated with chronic obstructive pulmonary disease (COPD). We investigated the molecular mechanism of lncRNA RP11-521C20.3, which targets the action of the Bcl-2 modifying factor (BMF) signaling pathway in the apoptosis of cigarette smoke extract (CSE)-treated A549 cells.Lung tissues derived from cigarette smoke exposed rats (COPD group) and controls were examined using TUNEL assay for apoptotic cells and using immunohistochemistry for BMF expression levels. Overexpression and knockdown of BMF by lentiviral vector transfection were used to explore the role of BMF on the apoptosis of CSE-treated A549 cells. Overexpression and knockdown of RP11-521C20.3 were used to assess the effect of RP11-521C20.3 on the expression levels of BMF and apoptosis in CSE-treated A549 cells. Cell proliferation, mitochondrial morphology, and apoptosis were assessed in A549 cells. Real-time quantitative polymerase chain reactions and Western blotting detected the expression of apoptosis-related molecules.The number of apoptotic cells and the level of BMF protein were significantly increased in lung tissues of the COPD group compared to the control group. Overexpression of BMF or knockdown of RP11-521C20.3 in CSE-treated A549 cells increased apoptosis, inhibited cell proliferation, and exacerbated mitochondrial damage. There were also increased protein levels of p53, cleaved caspase-3, and cleaved caspase-7, and decreased protein levels of Bcl-2 and survivin. Knockdown of BMF or overexpression of RP11-521C20.3 in CSE-treated A549 cells attenuated apoptosis, promoted cell proliferation, and alleviated mitochondrial damage. Observed effects also included decreased protein levels of p53, cleaved caspase-3, and cleaved caspase-7, and increased protein levels of Bcl-2 and survivin. In CSE-treated A549 cells, overexpression of RP11-521C20.3 suppressed the expression of BMF mRNA and protein.In CSE-treated A549 cells, BMF promoted apoptosis and RP11-521C20.3 might target the BMF signaling axis to protect CSE-treated A549 cells from apoptosis.© 2023 Zhong et al.

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大类 | 3 区医学

小类 | 3 区呼吸系统

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出版当年[2023]版：

Q2 RESPIRATORY SYSTEM

最新[2023]版：

Q2 RESPIRATORY SYSTEM

影响因子： 2.7 最新[2023版] 2.9 最新五年平均 2.7 出版当年[2023版] 2.9 出版当年五年平均 2.8 出版前一年[2022版]

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第一作者机构： [1]Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, People’s

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通讯机构： [1]Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, People’s [*1]Department of Respiratory Critical Care Medicine, the First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650032, People’s Republic of China

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LncRNA RP11-521C20.3 Inhibits Cigarette Smoke Extract-Induced Apoptosis in A549 Cells by Targeting BMF Signaling

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