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长链非编码 RNA LUADT1 通过下调 miR-1207-5p 促进鼻咽癌细胞的增殖和侵袭。

Long non-coding RNA LUADT1 promotes nasopharyngeal carcinoma cell proliferation and invasion by downregulating miR-1207-5p.

机构信息

Department of Radiation Oncology, The Affiliated Cancer Hospital of Nanjing Medical University & Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research, Nanjing, China.

Department of Medical Oncology, The Affiliated Cancer Hospital of Nanjing Medical University & Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research, Nanjing, China.

出版信息

Bioengineered. 2021 Dec;12(2):10716-10728. doi: 10.1080/21655979.2021.2001952.

Abstract

Nasopharyngeal carcinoma (NPC) is a typical type of malignant tumor. This research paper aims to study the function and mechanism of long non-coding RNA lung adenocarcinoma-related transcript 1 (lncRNA-LUADT1) in the progression of NPC. In this study, the expressions of lncRNA-LUADT1, miR-1207-5p, and TEAD1 in NPC tissues and cell lines were detected by RT-qPCR. Initially, the expression of lncRNA-LUADT1 and TEAD1 were significantly up-regulated in NPC tissues and cells, while miR-1207-5p was significantly down-regulated. Next, miR-1207-5p was confirmed to bind to lncRNA-LUADT1 or TEAD1 by bioinformatics and luciferase reporter assay. In addition, after interfering with lncRNA-LUADT1 expression, experiments of CCK8, EDU staining, and Transwell invasion were used to detect proliferation, invasion, and migration of NPC cells. The results showed that interfering with lncRNA-LUADT1 expression could inhibit the proliferation, invasion, and migration of NPC cells. Western blot showed that lncRNA-LUADT1 knockdown significantly decreased the expression of Hippo/YAP pathway protein (YAP1 and TAZ). However, interfering with the expression of miR-1207-5p reversed these results. In addition, the nude mouse tumor formation experiment suggested that low-expressed lncRNA-LUADT1 reduced the volume and weight of tumor tissues. In summary, lncRNA-LUADT1 down-regulation could inhibit NPC cell proliferation and invasion, which may be achieved through regulating miR-1207-5p expression and affecting TEAD1 expression, thus inhibiting the activation of Hippo/YAP signaling pathway.

摘要

鼻咽癌(NPC)是一种典型的恶性肿瘤。本研究旨在探讨长链非编码 RNA 肺腺癌相关转录本 1(lncRNA-LUADT1)在 NPC 进展中的功能和机制。本研究采用 RT-qPCR 检测 NPC 组织和细胞系中 lncRNA-LUADT1、miR-1207-5p 和 TEAD1 的表达。结果显示,NPC 组织和细胞中 lncRNA-LUADT1 和 TEAD1 的表达明显上调,而 miR-1207-5p 的表达明显下调。生物信息学和荧光素酶报告基因实验证实 miR-1207-5p 可与 lncRNA-LUADT1 或 TEAD1 结合。此外,干扰 lncRNA-LUADT1 表达后,通过 CCK8、EDU 染色和 Transwell 侵袭实验检测 NPC 细胞的增殖、侵袭和迁移能力。结果表明,干扰 lncRNA-LUADT1 表达可抑制 NPC 细胞的增殖、侵袭和迁移能力。Western blot 结果显示,lncRNA-LUADT1 敲低可显著降低 Hippo/YAP 通路蛋白(YAP1 和 TAZ)的表达。然而,干扰 miR-1207-5p 的表达可逆转这些结果。此外,裸鼠肿瘤形成实验表明,低表达 lncRNA-LUADT1 可降低肿瘤组织的体积和重量。综上所述,lncRNA-LUADT1 下调可抑制 NPC 细胞的增殖和侵袭,这可能是通过调节 miR-1207-5p 的表达并影响 TEAD1 的表达,从而抑制 Hippo/YAP 信号通路的激活来实现的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eff/8810096/d1a05886610c/KBIE_A_2001952_F0001_B.jpg

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