长链非编码 RNA MALAT1 通过海绵吸附 miR-129-5p 增加. 的表达调控支气管肺发育不良的发生

OBJECTIVE

To explore the function and mechanism of long noncoding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in bronchopulmonary dysplasia.

METHODS

Alveolar epithelial cell line BEAS-2B was used as the cell model. The role of MALAT1 and microRNA miR-129-5p in regulating cellular viability and migration were examined by using the CCK-8 and Transwell assays, respectively, in vitro. The luciferase reporter assay and real-time (RT)-PCR were performed to confirm that miR-129-5p was a target of MALAT1. ELISA was conducted to validate MALAT1 and show that miR-129-5p regulated the gene encoding high-mobility group protein 1 ().

RESULTS

Overexpression of MALAT1 significantly promoted cellular viability, whereas miR-129-5p had the opposite effect. miR-129-5p was shown to be a target of MALAT1, and HMGB1 could be upregulated by MALAT1 overexpression or miR-129-5p inhibition.

CONCLUSION

MALAT1 reduced the expression of miR-129-5p, promoting the viability of cells and blocking the development of bronchopulmonary dysplasia. In addition, MALAT1 increased the expression of HMGB1, which contributed to inflammation as the disease progressed.

目的

探讨长链非编码 RNA（lncRNA）肺腺癌转移相关转录本 1（MALAT1）在支气管肺发育不良中的作用及机制。

方法

以肺泡上皮细胞系 BEAS-2B 为细胞模型。采用 CCK-8 法和 Transwell 法分别检测 MALAT1 和微小 RNA miR-129-5p 对细胞活力和迁移的调节作用。采用荧光素酶报告基因检测和实时（RT）-PCR 验证 miR-129-5p 是 MALAT1 的靶点。ELISA 验证 MALAT1 并显示 miR-129-5p 调节高迁移率族蛋白 1（HMGB1）基因的表达。