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长链非编码RNA TRG-AS1通过吸附miR-4500调节BACH1来促进肝细胞癌进展。

LncRNA TRG-AS1 stimulates hepatocellular carcinoma progression by sponging miR-4500 to modulate BACH1.

作者信息

Sun Xuehu, Qian Yeben, Wang Xingyu, Cao Rongge, Zhang Jianlin, Chen Weidong, Fang Maoyong

机构信息

Department of Emergency Surgery, the First Affiliated Hospital of Anhui Medical University, Hefei, 230000 Anhui China.

Department of Hepatobiliary Surgery, the First Affiliated Hospital of Anhui Medical University, No.218 Jixi Road, Hefei, 230000 Anhui China.

出版信息

Cancer Cell Int. 2020 Aug 4;20:367. doi: 10.1186/s12935-020-01440-3. eCollection 2020.

DOI:10.1186/s12935-020-01440-3
PMID:32774161
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7401190/
Abstract

BACKGROUND

T cell receptor gamma locus antisense RNA 1 (TRG-AS1) has been reported to involve in the progression of glioblastoma, however the role and its underlying molecular mechanism in hepatocellular carcinoma (HCC) remain unknown.

METHODS

Quantitative real-time polymerase chain reaction (RT-qPCR) was applied to detect TRG-AS1 expression in HCC cells. Besides, the proliferation abilities of HCC cells were assessed by colony formation and EdU assays. The migratory and invasive abilities of HCC cells were examined by transwell assays. Imunofluorescence staining (IF) was used to analyze the epithelial-mesenchymal transitions (EMT). The interaction among TRG-AS1, miR-4500 and BTB domain and CNC homolog 1 (BACH1) were proofed by means of RIP and RNA pull down and luciferase reporter assays.

RESULTS

TRG-AS1 was conspicuously overexpressed in HCC cells. TRG-AS1 silencing apparently suppressed HCC cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT). Mechanism exploration revealed that TRG-AS1 acted as a molecular sponge of miR-4500 to regulate BACH1. MiR-4500 silencing or BACH1 overexpression in BACH1-downregulated cells fully rescued cell proliferation migration, invasion and EMT progress.

CONCLUSION

TRG-AS1 regulates HCC progression by targeting miR-4500/BACH1 axis.

摘要

背景

据报道，T细胞受体γ基因座反义RNA 1（TRG-AS1）参与胶质母细胞瘤的进展，但其在肝细胞癌（HCC）中的作用及其潜在分子机制尚不清楚。

方法

应用定量实时聚合酶链反应（RT-qPCR）检测HCC细胞中TRG-AS1的表达。此外，通过集落形成和EdU试验评估HCC细胞的增殖能力。通过Transwell试验检测HCC细胞的迁移和侵袭能力。免疫荧光染色（IF）用于分析上皮-间质转化（EMT）。通过RIP、RNA下拉和荧光素酶报告基因试验验证TRG-AS1、miR-4500和BTB结构域及CNC同源物1（BACH1）之间的相互作用。

结果

TRG-AS1在HCC细胞中明显过表达。TRG-AS1沉默明显抑制HCC细胞增殖、迁移、侵袭和上皮-间质转化（EMT）。机制探索表明，TRG-AS1作为miR-4500的分子海绵来调节BACH1。在BACH1下调的细胞中，miR-4500沉默或BACH1过表达完全挽救了细胞增殖、迁移、侵袭和EMT进程。

结论

TRG-AS1通过靶向miR-4500/BACH1轴调节HCC进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/7401190/1127b681586f/12935_2020_1440_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/7401190/b897bc4cac7a/12935_2020_1440_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/7401190/cdf052f5df60/12935_2020_1440_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/7401190/2e792d59f72b/12935_2020_1440_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/7401190/05ffdb6b8031/12935_2020_1440_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/7401190/cefb6cc5467d/12935_2020_1440_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/7401190/1127b681586f/12935_2020_1440_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/7401190/b897bc4cac7a/12935_2020_1440_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/7401190/cdf052f5df60/12935_2020_1440_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/7401190/2e792d59f72b/12935_2020_1440_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/7401190/05ffdb6b8031/12935_2020_1440_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/7401190/cefb6cc5467d/12935_2020_1440_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8d9/7401190/1127b681586f/12935_2020_1440_Fig6_HTML.jpg

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