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lncRNA PSMA3-AS1 通过靶向 miR-17-5p/PD-L1 促进非小细胞肺癌的进展。

lncRNA PSMA3-AS1 promotes the progression of non-small cell lung cancer through targeting miR-17-5p/PD-L1.

机构信息

Department of Oncology, Second Hospital of Shanxi Medical University, Taiyuan, China.

出版信息

Adv Clin Exp Med. 2021 Oct;30(10):1043-1050. doi: 10.17219/acem/138624.

DOI:10.17219/acem/138624
PMID:34610219
Abstract

BACKGROUND

A growing number of studies have shown that long-chain non-coding RNA (lncRNA) plays an important role in the progression of non-small cell lung cancer (NSCLC).

OBJECTIVES

To explore the role and potential molecular mechanism of lncRNA PSMA3-AS1 in promoting the proliferation, migration and invasion of NSCLC.

MATERIAL AND METHODS

The expression of PSMA3-AS1, miR-17-5p and PD-L1 in a human bronchial epithelial cell line, BEAS-2B, and NSCLC cell lines, H226 and A549, were detected with quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. The PSMA3-AS1 shRNA transfection was used to reduce the expression of PSMA3-AS1. Double fluorescent enzyme reporting was used to detect the relationship between PSMA3-AS1, miR-17-5p and PD-L1. Cell Counting Kit-8 (CCK-8), wound-healing and transwell assays, as well as western blot, were used to detect the expression of proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT)-related proteins in lung cancer cells.

RESULTS

The expression of PSMA3-AS1 in NSCLC cells was significantly higher than in human bronchial epithelial cells. The PSMA3-AS1 knockdown significantly reduced the proliferation, migration and invasion of lung cancer cells. In addition, double fluorescent enzyme results showed that PSMA3-AS1 could competitively bind miR-17-5p to PD-L1. The expression of miR-17-5p is low in lung cancer cells, while the expression of PD-L1 in them is high. Overexpression of PD-L1 reversed the inhibitory effect of PSMA3-AS1 knockdown on the proliferation, migration and invasion of lung cancer cells.

CONCLUSIONS

Generally speaking, PSMA3-AS1 is highly expressed in NSCLC. The PSMA3-AS1 can promote the proliferation, migration and invasion of NSCLC cells by regulating miR-17-5p/PD-L1.

摘要

背景

越来越多的研究表明,长链非编码 RNA(lncRNA)在非小细胞肺癌(NSCLC)的进展中发挥重要作用。

目的

探讨 lncRNA PSMA3-AS1 促进 NSCLC 增殖、迁移和侵袭的作用及潜在分子机制。

材料与方法

采用实时定量聚合酶链反应(qRT-PCR)或 Western blot 检测人支气管上皮细胞系 BEAS-2B 和 NSCLC 细胞系 H226 和 A549 中 PSMA3-AS1、miR-17-5p 和 PD-L1 的表达。采用 PSMA3-AS1 shRNA 转染降低 PSMA3-AS1 的表达。双荧光酶报告检测 PSMA3-AS1、miR-17-5p 和 PD-L1 之间的关系。细胞计数试剂盒-8(CCK-8)、划痕愈合和 Transwell 实验以及 Western blot 检测肺癌细胞增殖、迁移、侵袭和上皮-间充质转化(EMT)相关蛋白的表达。

结果

NSCLC 细胞中 PSMA3-AS1 的表达明显高于人支气管上皮细胞。PSMA3-AS1 敲低显著降低了肺癌细胞的增殖、迁移和侵袭。此外,双荧光酶结果表明 PSMA3-AS1 可以竞争性结合 miR-17-5p 来靶向 PD-L1。肺癌细胞中 miR-17-5p 的表达较低,而 PD-L1 的表达较高。过表达 PD-L1 逆转了 PSMA3-AS1 敲低对肺癌细胞增殖、迁移和侵袭的抑制作用。

结论

一般来说,PSMA3-AS1 在 NSCLC 中高表达。PSMA3-AS1 可通过调节 miR-17-5p/PD-L1 促进 NSCLC 细胞的增殖、迁移和侵袭。

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