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Livin通过lncRNA-ATB参与转化生长因子-β1诱导的肾小管上皮-间充质转化。

Livin is involved in TGF-β1-induced renal tubular epithelial-mesenchymal transition through lncRNA-ATB.

作者信息

Zhou Jieqing, Jiang Hong

机构信息

Department of Pediatrics, The First Hospital of China Medical University, Shenyang 110001, China.

出版信息

Ann Transl Med. 2019 Sep;7(18):463. doi: 10.21037/atm.2019.08.29.

DOI:10.21037/atm.2019.08.29
PMID:31700899
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6803240/
Abstract

BACKGROUND

Renal interstitial fibrosis is accepted as a crucial component of chronic kidney diseases (CKD). Epithelial-mesenchymal transition (EMT) is an important factor contributing to renal interstitial fibrosis. Livin, due to its ability to induce EMT, is an important regulator of many types of tumors and might also be involved in human renal tubular EMT.

METHODS

We confirmed that Livin and lncRNA-ATB could aggravate EMT and , lncRNA-ATB could be suppressed by the silencing of Livin whereas Livin expression was nearly stable when lncRNA-ATB was overexpressed or knocked out.

RESULTS

Livin was upregulated and at the similar rate as the occurrence of EMT, which could be relieved when Livin was silenced. LncRNA-ATB, which is another important regulator of EMT, was also found highly expressed during this process. The silencing of lncRNA-ATB could lessen the severity of EMT, and the overexpression of lncRNA-ATB could aggravate EMT without affecting the expression of Livin.

CONCLUSIONS

Livin promotes EMT through the regulation of lncRNA-ATB. The silencing of Livin might be an effective targeted therapy for renal fibrosis.

摘要

背景

肾间质纤维化被认为是慢性肾脏病(CKD)的关键组成部分。上皮-间质转化(EMT)是导致肾间质纤维化的一个重要因素。Livin因其诱导EMT的能力,是多种肿瘤的重要调节因子,也可能参与人类肾小管EMT。

方法

我们证实Livin和lncRNA-ATB可加重EMT,且lncRNA-ATB可被Livin沉默所抑制,而当lncRNA-ATB过表达或敲除时,Livin表达几乎稳定。

结果

Livin上调,且上调速率与EMT的发生相似,当Livin沉默时这种上调可得到缓解。lncRNA-ATB作为EMT的另一个重要调节因子,在此过程中也被发现高表达。lncRNA-ATB的沉默可减轻EMT的严重程度,lncRNA-ATB的过表达可加重EMT,而不影响Livin的表达。

结论

Livin通过调节lncRNA-ATB促进EMT。Livin的沉默可能是肾纤维化的一种有效靶向治疗方法。

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