Diagnostic value of LncRNA SNHG16 for osteoporotic fractures and its potential regulation of fracture healing.

IF 2.5 3区 生物学
Yuanming Luo, Qingfeng Zhang, Changqing Shao, Jin Li, Jiaojiao Chen, Liang Han, Xiaowei Jiang, Li Hong
{"title":"Diagnostic value of LncRNA SNHG16 for osteoporotic fractures and its potential regulation of fracture healing.","authors":"Yuanming Luo, Qingfeng Zhang, Changqing Shao, Jin Li, Jiaojiao Chen, Liang Han, Xiaowei Jiang, Li Hong","doi":"10.1186/s41065-025-00423-6","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Osteoporotic fractures (OPF) have a serious impact on the health of patients. It is of great importance to investigate the diagnostic effect of SNH16 on OPF and the mechanism of action to promote fracture healing.</p><p><strong>Methods: </strong>132 OPF patients and 128 OP patients were included. The levels of SNHG16, Col I, RUNX2 and OCN were evaluated by RT-qPCR. The diagnostic value of SNHG16 was evaluated by ROC curve. Cell proliferation ability was assessed by CCK-8, and apoptosis rate was detected by flow cytometry. ENCORI was used to predict the binding sites of SNHG16 with downstream target genes. DLR assay demonstrated the targeting relationship between SNHG16 and miR-432-5p.</p><p><strong>Results: </strong>SNHG16 was poorly expressed in OPF patients compared with OP patients, and its expression was lower in patients with delayed healing. In addition, in the OPF, OPG level was decreased, the level of RANKL was increased, and the balance of bone resorption formation is disrupted leading to fractures. Knockdown of SNHG16 results in decreased cell proliferation and increased apoptosis, and high SNHG16 expression decreases miR-432-5p expression, thereby increasing the levels of Col I, RUNX2 and OCN.</p><p><strong>Conclusion: </strong>Increasing SNHG16 can reduce the level of miR-432-5p thereby increasing the level of osteosynthesis proteins and restoring cellular activity, thereby promoting fracture healing.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"54"},"PeriodicalIF":2.5000,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11974092/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Hereditas","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1186/s41065-025-00423-6","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Osteoporotic fractures (OPF) have a serious impact on the health of patients. It is of great importance to investigate the diagnostic effect of SNH16 on OPF and the mechanism of action to promote fracture healing.

Methods: 132 OPF patients and 128 OP patients were included. The levels of SNHG16, Col I, RUNX2 and OCN were evaluated by RT-qPCR. The diagnostic value of SNHG16 was evaluated by ROC curve. Cell proliferation ability was assessed by CCK-8, and apoptosis rate was detected by flow cytometry. ENCORI was used to predict the binding sites of SNHG16 with downstream target genes. DLR assay demonstrated the targeting relationship between SNHG16 and miR-432-5p.

Results: SNHG16 was poorly expressed in OPF patients compared with OP patients, and its expression was lower in patients with delayed healing. In addition, in the OPF, OPG level was decreased, the level of RANKL was increased, and the balance of bone resorption formation is disrupted leading to fractures. Knockdown of SNHG16 results in decreased cell proliferation and increased apoptosis, and high SNHG16 expression decreases miR-432-5p expression, thereby increasing the levels of Col I, RUNX2 and OCN.

Conclusion: Increasing SNHG16 can reduce the level of miR-432-5p thereby increasing the level of osteosynthesis proteins and restoring cellular activity, thereby promoting fracture healing.

LncRNA SNHG16对骨质疏松性骨折的诊断价值及其对骨折愈合的潜在调控作用。
背景:骨质疏松性骨折严重影响患者的健康。探讨SNH16对OPF的诊断作用及促进骨折愈合的作用机制具有重要意义。方法:选取OPF患者132例,OP患者128例。RT-qPCR检测SNHG16、Col I、RUNX2、OCN的表达水平。采用ROC曲线评价SNHG16的诊断价值。CCK-8检测细胞增殖能力,流式细胞术检测细胞凋亡率。使用ENCORI预测SNHG16与下游靶基因的结合位点。DLR分析证实了SNHG16与miR-432-5p之间的靶向关系。结果:与OP患者相比,SNHG16在OPF患者中的表达较低,且在延迟愈合患者中的表达较低。此外,在OPF中,OPG水平降低,RANKL水平升高,骨吸收形成平衡被破坏,导致骨折。SNHG16敲低导致细胞增殖减少,细胞凋亡增加,SNHG16高表达降低miR-432-5p表达,从而升高Col I、RUNX2和OCN水平。结论:增加SNHG16可降低miR-432-5p水平,从而提高成骨蛋白水平,恢复细胞活性,促进骨折愈合。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Hereditas
Hereditas Biochemistry, Genetics and Molecular Biology-Genetics
CiteScore
3.80
自引率
3.70%
发文量
0
期刊介绍: For almost a century, Hereditas has published original cutting-edge research and reviews. As the Official journal of the Mendelian Society of Lund, the journal welcomes research from across all areas of genetics and genomics. Topics of interest include human and medical genetics, animal and plant genetics, microbial genetics, agriculture and bioinformatics.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信