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长链非编码RNA HCP5通过海绵化miR-29b-3p促进人膀胱癌细胞的侵袭和迁移。

LncRNA HCP5 Promotes Cell Invasion and Migration by Sponging miR-29b-3p in Human Bladder Cancer.

作者信息

Zhao Cheng, Li Yangle, Hu Xiheng, Wang Ruizhe, He Wei, Wang Long, Qi Lin, Tong Shiyu

机构信息

Department of Urology, Xiangya Hospital, Central South University, Changsha City, Hunan Province 410008, People's Republic of China.

出版信息

Onco Targets Ther. 2020 Nov 17;13:11827-11838. doi: 10.2147/OTT.S249770. eCollection 2020.

DOI:10.2147/OTT.S249770
PMID:33235469
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7680190/
Abstract

BACKGROUND

Bladder cancer (BC) is one of the most common malignant tumors in the urinary system. In this study, the roles of lncRNA HCP5 (human major histocompatibility complex p5) and miR-29b-3p in human BC were investigated. Their regulations involved in cell invasion and migration were also evaluated.

METHODS

Luciferase reporter assay was performed to detect the binding between miR-29b-3p and HCP5 or high-mobility group box 1 (HMGB1). Cell viability, migration, invasion and apoptosis were assessed by CCK-8, colony formation, transwell assay and flow cytometry, respectively. Expression levels of HMGB1/toll-like receptor 4 (TLR4) proteins were measured by Western blot. Xenograft model was built, and tumor volumes and weights were calculated.

RESULTS

The results revealed dysregulation of HCP5 and miR-29b-3p in BC samples and cells. HCP5 negatively regulated the expression of miR-29b-3p and enhanced cell viability, migration and invasion. MiR-29b-3p mediated the effect of HCP5 on cell viability, proliferation, migration and invasion in RT4 cells. In addition, miR-29b-3p could regulate the expression of HMGB1 through interaction with HMGB1.

CONCLUSION

The findings in this study supported that lncRNA HCP5 could promote cell invasion and migration by sponging miR-29b-3p in human BC.

摘要

背景

膀胱癌(BC)是泌尿系统最常见的恶性肿瘤之一。在本研究中,探讨了长链非编码RNA HCP5(人类主要组织相容性复合体p5)和miR-29b-3p在人类膀胱癌中的作用。还评估了它们在细胞侵袭和迁移中的调控作用。

方法

进行荧光素酶报告基因检测以检测miR-29b-3p与HCP5或高迁移率族蛋白B1(HMGB1)之间的结合。分别通过CCK-8、集落形成、Transwell检测和流式细胞术评估细胞活力、迁移、侵袭和凋亡。通过蛋白质印迹法测量HMGB1/Toll样受体4(TLR4)蛋白的表达水平。建立异种移植模型,并计算肿瘤体积和重量。

结果

结果显示膀胱癌样本和细胞中HCP5和miR-29b-3p表达失调。HCP5负向调节miR-29b-3p的表达并增强细胞活力、迁移和侵袭。miR-29b-3p介导HCP5对RT4细胞中细胞活力、增殖、迁移和侵袭的影响。此外,miR-29b-3p可通过与HMGB1相互作用调节HMGB1的表达。

结论

本研究结果支持长链非编码RNA HCP5可通过在人类膀胱癌中海绵化miR-29b-3p促进细胞侵袭和迁移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bce/7680190/4e93dd1d8f23/OTT-13-11827-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bce/7680190/81007271faf8/OTT-13-11827-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bce/7680190/73cd7a3dbe6b/OTT-13-11827-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bce/7680190/d73efb2b4fd7/OTT-13-11827-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bce/7680190/ed013cfbe0fd/OTT-13-11827-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bce/7680190/6e4bdddb1df1/OTT-13-11827-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bce/7680190/4e93dd1d8f23/OTT-13-11827-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bce/7680190/81007271faf8/OTT-13-11827-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bce/7680190/73cd7a3dbe6b/OTT-13-11827-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bce/7680190/d73efb2b4fd7/OTT-13-11827-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bce/7680190/ed013cfbe0fd/OTT-13-11827-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bce/7680190/6e4bdddb1df1/OTT-13-11827-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bce/7680190/4e93dd1d8f23/OTT-13-11827-g0006.jpg

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