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长链非编码RNA NEAT1通过miR-524-5p/HDAC1轴抑制PTEN的乙酰化，从而促进喉癌细胞的增殖和侵袭。

Long noncoding RNA NEAT1 inhibits the acetylation of PTEN through the miR-524-5p /HDAC1 axis to promote the proliferation and invasion of laryngeal cancer cells.

作者信息

Zhang Jiajia, Wang Ping, Cui Yanli

机构信息

Department of Laboratory, The Affiliated Hospital of Henan Polytechnic University, The Second People's Hospital of Jiaozuo, Jiaozuo 454001, Henan, P.R. China.

Department of Hematology, The Affiliated Hospital of Henan Polytechnic University, The Second People's Hospital of Jiaozuo, Jiaozuo 454001, Henan, P.R. China.

出版信息

Aging (Albany NY). 2021 Nov 27;13(22):24850-24865. doi: 10.18632/aging.203719.

DOI:10.18632/aging.203719
PMID:34837887
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8660614/
Abstract

Long noncoding RNA nuclear paraspeckle assembly transcript 1 (lncRNA NEAT1) is abnormally expressed in numerous tumors and functions as an oncogene, but the role of NEAT1 in laryngocarcinoma is largely unknown. Our study validated that NEAT1 expression was markedly upregulated in laryngocarcinoma tissues and cells. Downregulation of NEAT1 dramatically suppressed cell proliferation and invasion through inhibiting miR-524-5p expression. Additionally, NEAT1 overexpression promoted cell growth and metastasis, while overexpression of miR-524-5p could reverse the effect. NEAT1 increased the expression of histone deacetylase 1 gene (HDAC1) via sponging miR-524-5p. Mechanistically, overexpression of HDAC1 recovered the cancer-inhibiting effects of miR-524-5p mimic or NEAT1 silence by deacetylation of tensin homolog deleted on chromosome ten (PTEN) and inhibiting AKT signal pathway. Moreover, experiments indicated that silence of NEAT1 signally suppressed tumor growth. Taken together, knockdown of NEAT1 suppressed laryngocarcinoma cell growth and metastasis by miR-524-5p/HDAC1/PTEN/AKT signal pathway, which provided a potential therapeutic target for laryngocarcinoma.

摘要

长链非编码RNA核副斑点组装转录本1（lncRNA NEAT1）在多种肿瘤中异常表达并发挥癌基因作用，但NEAT1在喉癌中的作用尚不清楚。我们的研究证实，NEAT1在喉癌组织和细胞中表达明显上调。下调NEAT1通过抑制miR-524-5p的表达显著抑制细胞增殖和侵袭。此外，NEAT1过表达促进细胞生长和转移，而miR-524-5p过表达可逆转这种作用。NEAT1通过吸附miR-524-5p增加组蛋白去乙酰化酶1基因（HDAC1）的表达。机制上，HDAC1过表达通过使第10号染色体缺失的张力蛋白同源物（PTEN）去乙酰化并抑制AKT信号通路，恢复了miR-524-5p模拟物或NEAT1沉默的抑癌作用。此外，实验表明沉默NEAT1显著抑制肿瘤生长。综上所述，敲低NEAT1通过miR-524-5p/HDAC1/PTEN/AKT信号通路抑制喉癌细胞生长和转移，为喉癌提供了一个潜在的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/740c/8660614/ab64ec269dce/aging-13-203719-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/740c/8660614/305d1ef07b68/aging-13-203719-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/740c/8660614/e91f38749e41/aging-13-203719-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/740c/8660614/9426cc08063b/aging-13-203719-g005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/740c/8660614/9604ff0e50a8/aging-13-203719-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/740c/8660614/04b5f340f629/aging-13-203719-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/740c/8660614/ab64ec269dce/aging-13-203719-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/740c/8660614/305d1ef07b68/aging-13-203719-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/740c/8660614/4a6b2a566d53/aging-13-203719-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/740c/8660614/e91f38749e41/aging-13-203719-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/740c/8660614/9604ff0e50a8/aging-13-203719-g007.jpg
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