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Hsa_circ_0091579/miR-940/TACR1轴调控肝细胞癌的发展。

The Hsa_circ_0091579/miR-940/TACR1 Axis Regulates the Development of Hepatocellular Carcinoma.

作者信息

Jiang Peiqiang, Han Wei, Fu Yu, Chen Qingmin

机构信息

Department of Hepatobiliary and Pancreatic Surgery, The First Hospital of Jilin University, Changchun, Jilin, People's Republic of China.

出版信息

Cancer Manag Res. 2020 Sep 28;12:9087-9096. doi: 10.2147/CMAR.S259243. eCollection 2020.

DOI:10.2147/CMAR.S259243
PMID:33061603
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7532044/
Abstract

PURPOSE

Circular RNAs (circRNAs) play important roles in hepatocellular carcinoma (HCC) development. The circRNA () is dysregulated in HCC, while the mechanism of in HCC development is largely unknown.

PATIENTS AND METHODS

Thirty paired cancer and adjacent normal tissues were harvested from HCC patients. SNU-387 and Huh7 cells were cultured in this study. , () and () abundances were measured via quantitative reverse transcription-polymerase chain reaction or Western blot. Cell viability, migration, invasion, colony ability, cell cycle distribution and apoptosis were assessed via 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide, transwell assay, colony formation assay and flow cytometry. The interaction among , and was tested via dual-luciferase reporter analysis. The anti-HCC role of knockdown in vivo was investigated using xenograft model.

RESULTS

expression was enhanced in HCC tissue samples and cells. silence inhibited cell viability, migration, invasion and colony formation, induced cell cycle arrest at G0/G1 phase, and promoted apoptosis in HCC cells. was targeted via and knockdown reversed the suppressive effect of silence on HCC development. targeted to repress HCC development. could regulate expression by mediating . Down-regulation of decreased xenograft tumor growth.

CONCLUSION

Knockdown of repressed HCC development by mediating / axis, indicating a new pathogenesis of HCC.

摘要

目的

环状RNA（circRNAs）在肝细胞癌（HCC）发展中发挥重要作用。circRNA（）在HCC中表达失调，但其在HCC发展中的机制尚不清楚。

患者和方法

从HCC患者中收集30对癌组织和癌旁正常组织。本研究培养了SNU - 387和Huh7细胞。通过定量逆转录 - 聚合酶链反应或蛋白质免疫印迹法检测（）、（）和（）的丰度。通过3 -（4,5 - 二甲基 - 2 - 噻唑基）- 2,5 - 二苯基 - 2 - H - 四氮唑溴盐、Transwell实验、集落形成实验和流式细胞术评估细胞活力、迁移、侵袭、集落形成能力、细胞周期分布和凋亡。通过双荧光素酶报告基因分析检测、和之间的相互作用。使用异种移植模型研究敲低在体内的抗HCC作用。

结果

在HCC组织样本和细胞中表达增强。沉默抑制细胞活力、迁移、侵袭和集落形成，诱导细胞周期停滞在G0/G1期，并促进HCC细胞凋亡。通过靶向，敲低可逆转沉默对HCC发展的抑制作用。靶向以抑制HCC发展。可通过介导调节的表达。下调可降低异种移植肿瘤的生长。

结论

敲低通过介导/轴抑制HCC发展，提示HCC的一种新发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9511/7532044/5c17bcac2e8d/CMAR-12-9087-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9511/7532044/99d129e334a5/CMAR-12-9087-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9511/7532044/7100aac2f58a/CMAR-12-9087-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9511/7532044/d986e876bfbe/CMAR-12-9087-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9511/7532044/f0bc70323e93/CMAR-12-9087-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9511/7532044/1e2e02664f27/CMAR-12-9087-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9511/7532044/5c17bcac2e8d/CMAR-12-9087-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9511/7532044/99d129e334a5/CMAR-12-9087-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9511/7532044/7100aac2f58a/CMAR-12-9087-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9511/7532044/d986e876bfbe/CMAR-12-9087-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9511/7532044/f0bc70323e93/CMAR-12-9087-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9511/7532044/1e2e02664f27/CMAR-12-9087-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9511/7532044/5c17bcac2e8d/CMAR-12-9087-g0006.jpg

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