Background

Pulmonary fibrosis is a serious clinical fatal disease. Epithelial–mesenchymal transition (EMT) and lncRNA NEAT1 have been implied in its development and progression.

Objective

To study the role of lncRNA NEAT1 in the progression of fibrosis in human pulmonary epithelial cells (BEAS-2B). Specifically, BEAS-2B was transfected with NEAT1 and miR-29c, EMT and cell proliferation were measured and the expression level of relevant genes was determined by Western blot.

Result

Results showed that NEAT1 promotes fibrosis and proliferation of BEAS-2B cells via the up-regulation of α-SMA, Vimentin, Snail and proliferation-related genes including Cyclin D1 and Cyclin E; miR-29c is a target gene of NEAT1 and through which NEAT1 regulates EMT and expression of proliferation-related genes.

Conclusion

This study investigated the mechanism of pulmonary fibrosis progression by elucidating the role of NEAT1/miR-29c in the fibrosis and proliferation of BEAS-2B cells, thus providing a basis for the new therapeutic targets of pulmonary fibrosis.

中文翻译：

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lncRNA NEAT1在肺上皮细胞纤维化中的作用和机制

背景

肺纤维化是一种严重的临床致命疾病。上皮-间质转化（EMT）和lncRNA NEAT1已暗示其发展和进程。

目的

研究lncRNA NEAT1在人肺上皮细胞（BEAS-2B）纤维化进程中的作用。具体地，用NEAT1和miR-29c转染BEAS-2B，测量EMT和细胞增殖，并通过Western印迹测定相关基因的表达水平。

结果

结果表明，NEAT1通过上调α-SMA，波形蛋白，Snail和增殖相关基因（包括Cyclin D1和Cyclin E）促进BEAS-2B细胞的纤维化和增殖。miR-29c是NEAT1的靶基因，NEAT1通过它调控EMT和增殖相关基因的表达。

结论

本研究通过阐明NEAT1 / miR-29c在BEAS-2B细胞纤维化和增殖中的作用，研究了肺纤维化进展的机制，从而为新的肺纤维化治疗靶标提供了基础。