Circ_LRP6 facilitates osteosarcoma progression via the miR‐122‐5p/miR‐204‐5p/HMGB1 axis

Author:

Wang Guanghui1,Wei Xiyuan2,Gao Shan1,Chen Wenheng1,Geng Yang1,Liu Jia3,Guan Hongya3ORCID

Affiliation:

1. Department of Orthopedic Surgery Zhumadian Central Hospital Zhumadian Henan China

2. Department of Medical Services Division Zhumadian Central Hospital Zhumadian Henan China

3. Research of Trauma Center Zhengzhou Central Hospital Affiliated to Zhengzhou University Zhengzhou China

Abstract

AbstractCirc_LRP6 is participated in the occurrence and development of numerous tumors. Nevertheless, its roles and mechanism in osteosarcoma (OS) is unknown. This study aims to illustrate this point. With the use of qRT‐PCR, the level of circ_LRP6, miR‐122‐5p, miR‐204‐5p and HMGB1 was identified. To observe cell proliferation, migration and invasion, we adopted CCK‐8 and Transwell assays in the present study. Besides, to prove the existing interaction, bioinformatics analysis and dual luciferase reporting assays were employed. The influence of circ_LRP6 on osteosarcoma in vivo was evaluated by subcutaneous tumor formation model in nude mice. In osteosarcoma tissues, circ_LRP6 and HMGB1 are strongly denoted, whereas miR‐122‐5p and miR‐204‐5p are under‐expressed. Circ_LRP6 knockdown could significantly hinder the proliferation, migration and invasion of osteosarcoma cells. Circ_LRP6 hindered the proliferation of osteosarcoma in vivo. Bioinformatics predicted that miR‐122‐5p and miR‐204‐5p functioned as direct targets of circ_LRP6, and HMGB1 were possible target genes of miR‐122‐5p and miR‐204‐5p. The findings indicated that the low level of miR‐122‐5p and miR‐204‐5p and the overexpression of HMGB1 could partially restore and reduce the inhibitory impact of circ_LRP6 on the proliferation, migration and invasion of osteosarcoma cells. Circ_LRP6 affects osteosarcoma progression via the miR‐122‐5p/miR‐204‐5p/HMGB1 axis, and is shown to be a molecular biomarker.

Publisher

Wiley

Subject

Health, Toxicology and Mutagenesis,Management, Monitoring, Policy and Law,Toxicology,General Medicine

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3