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LINC01433 靶向 miR-506-3p 促进鼻咽癌细胞的生物学进展。

LINC01433 targets miR-506-3p to promote the biological progress of nasopharyngeal carcinoma cells.

机构信息

Department of Otorhinolaryngology Head and Neck Surgery, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, No.3, East Qingchun Road, Hangzhou, 310016, Zhejiang Province, China.

出版信息

Eur Arch Otorhinolaryngol. 2021 Sep;278(9):3363-3374. doi: 10.1007/s00405-021-06607-w. Epub 2021 Jan 21.

DOI:10.1007/s00405-021-06607-w
PMID:33479848
Abstract

PURPOSE

The current study aimed to investigate the role of long intergenic noncoding 01433 (LINC01433) in the proliferation, migration and invasion of nasopharyngeal carcinoma (NPC).

METHODS

Real-time quantitative PCR (RT-qPCR) was performed to determine the expressions of LINC01433 and miR-506-3p in NPC samples and cell lines. The effects of LINC01433 on cell proliferation, migration and invasion were measured by CCK-8, wound healing assay and Transwell, respectively. In addition, Pearson correlation analysis, starBase, RNA immunoprecipitation, luciferase assay, Western blot and functional experiments were conducted to detect and confirm the relationship between LINC01433 and miR-506-3p.

RESULTS

LINC01433 level was noticeably elevated in NPC tissues and cell lines. As the expression of LINC01433 in 5-8F cells was the highest in NPC cell lines and the expression of LINC01433 in SUNE1 cells was the lowest, 5-8F and SUNE1 cells were therefore selected as the target cells for following experiments. Furthermore, miR-506-3p was predicted as the target of LINC01433, and the two were negatively correlated with each other. Interestingly, overexpression of LINC01433 promoted proliferation, migration and invasion of NPC cells, while miR-506-3p reversed such effects of LINC01433. Moreover, LINC01433 silencing had the opposite effects to LINC01433 overexpression. Furthermore, miR-506-3p overexpression inhibited the expressions of MMP2, N-cadherin, p-PI3K and p-Akt, and promoted the expressions of E-cadherin and TIMP-2, and partially reversed the role of LINC01433 in promoting cancer development.

CONCLUSION

The current findings reveal that LINC01433 regulates NPC cell biological progress through miR-506-3p.

摘要

目的

本研究旨在探讨长链非编码 RNA 01433(LINC01433)在鼻咽癌(NPC)增殖、迁移和侵袭中的作用。

方法

采用实时定量 PCR(RT-qPCR)检测 NPC 组织和细胞系中 LINC01433 和 miR-506-3p 的表达。通过 CCK-8 法、划痕愈合实验和 Transwell 实验分别测定 LINC01433 对细胞增殖、迁移和侵袭的影响。此外,还进行了 Pearson 相关性分析、starBase、RNA 免疫沉淀、荧光素酶报告基因检测、Western blot 和功能实验,以检测和证实 LINC01433 与 miR-506-3p 之间的关系。

结果

LINC01433 在 NPC 组织和细胞系中表达明显上调。在 NPC 细胞系中,5-8F 细胞中 LINC01433 的表达最高,而在 SUNE1 细胞中 LINC01433 的表达最低,因此选择 5-8F 和 SUNE1 细胞作为后续实验的靶细胞。此外,miR-506-3p 被预测为 LINC01433 的靶基因,两者呈负相关。有趣的是,过表达 LINC01433 促进 NPC 细胞的增殖、迁移和侵袭,而 miR-506-3p 则逆转了 LINC01433 的这种作用。此外,LINC01433 沉默具有与过表达 LINC01433 相反的作用。此外,miR-506-3p 过表达抑制 MMP2、N-钙黏蛋白、p-PI3K 和 p-Akt 的表达,促进 E-钙黏蛋白和 TIMP-2 的表达,并部分逆转了 LINC01433 促进癌症发展的作用。

结论

本研究结果表明,LINC01433 通过 miR-506-3p 调节 NPC 细胞的生物学进程。

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