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长链非编码RNA PVT1在甲状腺癌中作为肿瘤促进因子，并通过介导miR-423-5p-PAK3促进肿瘤进展。

LncRNA PVT1 Acts as a Tumor Promoter in Thyroid Cancer and Promotes Tumor Progression by Mediating miR-423-5p-PAK3.

作者信息

Lin Qiu-Yu, Qi Qian-Le, Hou Sen, Chen Zhen, Zhang Laney, Zhao Hong-Guang, Lin Cheng-He

机构信息

Nuclear Medicine Department, The First Hospital of Jilin University, Changchun City 130000, Jilin Province, People's Republic of China.

Chengdu Xinke Pharmaceutical Co., LTD, Chengdu City 610000, Sichuan Province, People's Republic of China.

出版信息

Cancer Manag Res. 2020 Dec 30;12:13403-13413. doi: 10.2147/CMAR.S283443. eCollection 2020.

DOI:10.2147/CMAR.S283443
PMID:33408513
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7779291/
Abstract

INTRODUCTION

Thyroid cancer (TC) is an endocrine tumor whose risk of onset has been rising, so the deep understanding of its molecular mechanism helps formulate new treatment strategies.

METHODS

This paper was aimed at exploring the regulatory mechanism of long non-coding RNA (LncRNA) plasmacytoma variant translocation 1 (PVT1) in TC. The expression of PVT1, miR-423-5p and p21-activated kinase 3 (PAK3) in TC tissues and cell lines was detected by real-time PCR. PAK3 levels were detected by Western blot. Regulatory relationships between target genes and the proliferation, invasion and apoptosis of cells and genes were analyzed.

RESULTS

PVT1 and PAK3 upregulated while miR-423-5p downregulated in the tissues and cell lines. PVT1 downregulation inhibited TC cells from malignantly proliferating and invading, and promoted their apoptosis. PVT1 specifically regulated miR-423-5p, and its overexpression could weaken the anti-tumor effect of this miR on TC cells. In addition, miR-423-5p directly targeted PAK3, and knocking down its expression could weaken the inhibitory effect of PAK3 downregulation on TC progression. Besides, PVT1 acted as a competitive endogenous RNA to sponge this miR and thus regulate PAK3 expression.

DISCUSSION

In conclusion, PVT1 can mediate the molecular mechanism of the miR-423-5p-PAK3 axis regulatory network on regulating TC, so it is a new direction of treating the disease.

摘要

引言

甲状腺癌（TC）是一种内分泌肿瘤，其发病风险一直在上升，因此深入了解其分子机制有助于制定新的治疗策略。

方法

本文旨在探讨长链非编码RNA（LncRNA）浆细胞瘤变异易位1（PVT1）在甲状腺癌中的调控机制。通过实时定量PCR检测甲状腺癌组织和细胞系中PVT1、miR-423-5p和p21激活激酶3（PAK3）的表达。通过蛋白质印迹法检测PAK3水平。分析靶基因与细胞增殖、侵袭和凋亡以及基因之间的调控关系。

结果

在组织和细胞系中，PVT1和PAK3上调，而miR-423-5p下调。PVT1下调抑制甲状腺癌细胞的恶性增殖和侵袭，并促进其凋亡。PVT1特异性调控miR-423-5p，其过表达可削弱该miR对甲状腺癌细胞的抗肿瘤作用。此外，miR-423-5p直接靶向PAK3，敲低其表达可削弱PAK3下调对甲状腺癌进展的抑制作用。此外，PVT1作为竞争性内源性RNA来吸附该miR，从而调节PAK3表达。

讨论

总之，PVT1可介导miR-423-5p-PAK3轴调控网络对甲状腺癌的分子调控机制，因此是治疗该疾病的一个新方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6804/7779291/8d6c6e8e2ba7/CMAR-12-13403-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6804/7779291/2d83e4f9e226/CMAR-12-13403-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6804/7779291/c5b81514ea82/CMAR-12-13403-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6804/7779291/c80d9b81febb/CMAR-12-13403-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6804/7779291/6a08eff91da4/CMAR-12-13403-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6804/7779291/6fe9de4c4583/CMAR-12-13403-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6804/7779291/8d6c6e8e2ba7/CMAR-12-13403-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6804/7779291/2d83e4f9e226/CMAR-12-13403-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6804/7779291/c5b81514ea82/CMAR-12-13403-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6804/7779291/c80d9b81febb/CMAR-12-13403-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6804/7779291/6a08eff91da4/CMAR-12-13403-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6804/7779291/6fe9de4c4583/CMAR-12-13403-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6804/7779291/8d6c6e8e2ba7/CMAR-12-13403-g0006.jpg

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