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长链非编码RNA ZNF667-AS1通过调控微小RNA-1290介导的PRUNE2来延缓食管鳞状细胞癌的发展。

Long non-coding RNA ZNF667-AS1 retards the development of esophageal squamous cell carcinoma via modulation of microRNA-1290-mediated PRUNE2.

作者信息

Zheng Ying-Juan, Liang Tian-Song, Wang Juan, Zhao Jing-Yi, Zhai Su-Nan, Yang Dao-Ke, Wang Li-Dong

机构信息

State Key Laboratory of Esophageal Cancer Prevention & Treatment, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, PR China.

Department of Radiotherapy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, PR China.

出版信息

Transl Oncol. 2022 Jul;21:101371. doi: 10.1016/j.tranon.2022.101371. Epub 2022 Apr 30.

DOI:10.1016/j.tranon.2022.101371
PMID:35504176
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9079108/
Abstract

Abnormal long non-coding RNAs (lncRNAs) have been detected in esophageal squamous cell carcinoma (ESCC). Here, we focused on lncRNA ZNF667-AS1 and its downstream mechanism in ESCC progression. Differentially expressed lncRNAs in ESCC were predicted by bioinformatics analysis. ZNF667-AS1, microRNA-1290 (miR-1290), and prune homolog 2 with BCH domain (PRUNE2) expression was determined with their relationship in cell biological processes analyzed also by means of gain- and loss-of-function assays. Xenograft mouse models were performed to re-produce the in vitro findings. We found a decline in ZNF667-AS1 expression in ESCC tissues and cell lines. ZNF667-AS1 overexpression indicated a favorable prognosis of ESCC sufferers. ZNF667-AS1 overexpression suppressed ESCC cell malignant potentials. ZNF667-AS1 reduced miR-1290 to result in upregulation of the miR-1290 target gene PRUNE2. The inhibiting property of ZNF667-AS1 on the malignant characteristics of ESCC cells was achieved by disrupting the miR-1290-mediated downregulation of PRUNE2. ZNF667-AS1 suppressed the tumorigenesis of ESCC in vivo. Collectively, our study demonstrates that ZNF667-AS1 can function as a tumor suppressor in ESCC by upregulating PRUNE2 and downregulating miR-1290.

摘要

在食管鳞状细胞癌（ESCC）中已检测到异常的长链非编码RNA（lncRNA）。在此，我们聚焦于lncRNA ZNF667-AS1及其在ESCC进展中的下游机制。通过生物信息学分析预测ESCC中差异表达的lncRNA。测定了ZNF667-AS1、微小RNA-1290（miR-1290）和含BCH结构域的剪接因子2同源物（PRUNE2）的表达，并通过功能获得和功能缺失实验分析了它们在细胞生物学过程中的关系。建立了异种移植小鼠模型以重现体外实验结果。我们发现ESCC组织和细胞系中ZNF667-AS1表达下降。ZNF667-AS1过表达表明ESCC患者预后良好。ZNF667-AS1过表达抑制ESCC细胞的恶性潜能。ZNF667-AS1降低miR-1290水平，导致miR-1290靶基因PRUNE2上调。ZNF667-AS1对ESCC细胞恶性特征的抑制作用是通过破坏miR-1290介导的PRUNE2下调实现的。ZNF667-AS1在体内抑制ESCC的肿瘤发生。总的来说，我们的研究表明ZNF667-AS1在ESCC中可通过上调PRUNE2和下调miR-1290发挥肿瘤抑制作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40eb/9079108/78306cd4c94c/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40eb/9079108/cf2c41c60931/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40eb/9079108/704a7c7fadff/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40eb/9079108/38a091c74666/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40eb/9079108/d44b238dc79e/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40eb/9079108/7ba404d2be2f/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40eb/9079108/4fa7dd8acb85/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40eb/9079108/78306cd4c94c/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40eb/9079108/cf2c41c60931/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40eb/9079108/704a7c7fadff/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40eb/9079108/38a091c74666/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40eb/9079108/d44b238dc79e/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40eb/9079108/7ba404d2be2f/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40eb/9079108/4fa7dd8acb85/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40eb/9079108/78306cd4c94c/gr7.jpg

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