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长链非编码RNA SNHG6通过在食管鳞状细胞癌中吸附miR-101-3p来调节EZH2表达从而抑制细胞凋亡。

LncRNA SNHG6 Inhibits Apoptosis by Regulating EZH2 Expression via the Sponging of MiR-101-3p in Esophageal Squamous-Cell Carcinoma.

作者信息

Wang Jiang, Yang Xiaorui, Li Ruijia, Zhang Rui, Hu Desheng, Zhang Yueli, Gao Lei

机构信息

Department of Gastrointestinal Surgery, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, People's Republic of China.

Department of Clinical Pharmacy, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou, People's Republic of China.

出版信息

Onco Targets Ther. 2020 Nov 6;13:11411-11420. doi: 10.2147/OTT.S275135. eCollection 2020.

DOI:10.2147/OTT.S275135
PMID:33192074
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7656962/
Abstract

BACKGROUND

The long non-coding RNA (lncRNA) SNHG6 was significantly upregulated in esophageal squamous-cell carcinoma (ESCC), and it promoted ESCC cell proliferation, invasion, and migration. However, the effects of SNHG6 on cell apoptosis and the corresponding underlying mechanisms have not yet reported.

METHODS

Apoptosis was detected by flow cytometric analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were used for mRNA and protein quantification, respectively. A luciferase reporter assay was performed to verify downstream target genes for SNHG6 and miR-101-3p.

RESULTS

Dysregulation of SNHG6 inhibited apoptosis in ESCC cells and regulated the expression of apoptosis-related proteins such as Bcl-2, Mcl-1, Bax and Caspase-3. Functionally, miR-101-3p could compete binding with 3'-untranslated region of SNHG6 and downregulation of miR-101-3p reversed its effect on cell apoptosis in SNHG6 knockdown cells. was confirmed as a downstream target gene of miR-101-3p, silencing expression had the same effect on apoptosis and protein expression as knocking down SNHG6. Overexpression of reversed the effects of miR-101-3p overexpression on cell apoptosis in ESCC cells.

CONCLUSION

In this study, we found that upregulation of the lncRNA SNHG6 inhibited apoptosis via miR-101-3p/ axis in ESCC. These findings may contribute to the diagnosis and treatment of ESCC.

摘要

背景

长链非编码RNA（lncRNA）SNHG6在食管鳞状细胞癌（ESCC）中显著上调，且促进ESCC细胞增殖、侵袭和迁移。然而，SNHG6对细胞凋亡的影响及相应潜在机制尚未见报道。

方法

通过流式细胞术分析检测细胞凋亡。分别采用定量实时聚合酶链反应（qRT-PCR）和蛋白质免疫印迹法进行mRNA和蛋白质定量分析。进行荧光素酶报告基因检测以验证SNHG6和miR-101-3p的下游靶基因。

结果

SNHG6失调抑制ESCC细胞凋亡，并调节凋亡相关蛋白如Bcl-2、Mcl-1、Bax和Caspase-3的表达。在功能上，miR-101-3p可与SNHG6的3'-非翻译区竞争性结合，miR-101-3p下调可逆转其对SNHG6敲低细胞中细胞凋亡的影响。被证实为miR-101-3p的下游靶基因，沉默表达对细胞凋亡和蛋白质表达的影响与敲低SNHG6相同。的过表达可逆转miR-101-3p过表达对ESCC细胞凋亡的影响。

结论

在本研究中，我们发现lncRNA SNHG6上调通过miR-101-3p/轴抑制ESCC细胞凋亡。这些发现可能有助于ESCC的诊断和治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/163d/7656962/25de78200ba8/OTT-13-11411-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/163d/7656962/2cc4972e4aac/OTT-13-11411-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/163d/7656962/91cb6dc926cc/OTT-13-11411-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/163d/7656962/6240c961cf6d/OTT-13-11411-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/163d/7656962/792087911be9/OTT-13-11411-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/163d/7656962/25de78200ba8/OTT-13-11411-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/163d/7656962/2cc4972e4aac/OTT-13-11411-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/163d/7656962/91cb6dc926cc/OTT-13-11411-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/163d/7656962/6240c961cf6d/OTT-13-11411-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/163d/7656962/792087911be9/OTT-13-11411-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/163d/7656962/25de78200ba8/OTT-13-11411-g0005.jpg

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