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LINC00339 在延迟性骨折愈合中的功能机制及临床意义。

Functional mechanism and clinical implications of LINC00339 in delayed fracture healing.

机构信息

Department of Integrated Traditional Chinese and Western Medicine, Tianjin Hospital, Tianjin, 300211, China.

Department of Breast Oncology, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.

出版信息

J Orthop Surg Res. 2024 Aug 27;19(1):511. doi: 10.1186/s13018-024-04998-0.

DOI:10.1186/s13018-024-04998-0
PMID:39192334
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11348643/
Abstract

OBJECTIVE

Delayed fracture healing is a common complication of fractures that significantly impacts human health. This study aimed to explore the role of LINC00339 (lncRNA) in delayed fracture healing to provide new directions for its treatment.

METHODS

This study included 82 patients with fractures healing in a normal manner and 90 patients experiencing delayed fracture healing. Levels of LINC00339, miR-16-5p, and osteogenic marker-related mRNAs were measured using RT-qPCR. The predictive potential of LINC00339 for delayed fracture healing was validated using ROC curve analysis. The interaction between LINC00339 and miR-16-5p was validated using dual-luciferase reporter assays and RIP experiments. CCK-8 was used to assess cell proliferation, and apoptosis rates were measured by flow cytometry.

RESULTS

LINC00339 was significantly upregulated in delayed fracture healing patients and exhibited strong predictive ability for this condition. Overexpression of LINC00339 inhibited osteoblast proliferation, promoted apoptosis, and reduced mRNA levels of osteogenic markers (P < 0.05). miR-16-5p was recognized as a target mRNA of LINC00339, with LINC00339 exerting negative regulation on miR-16-5p, while overexpression of miR-16-5p mitigated the inhibitory effects of LINC00339 on fracture healing (P < 0.05).

CONCLUSION

This research indicated that LINC00339 may serve as a diagnostic marker for delayed fracture healing and revealed the function of the LINC00339/miR-16-5p axis on fracture healing by regulating osteoblasts.

摘要

目的

骨折延迟愈合是骨折的一种常见并发症，严重影响人类健康。本研究旨在探讨 LINC00339（lncRNA）在骨折延迟愈合中的作用，为其治疗提供新的方向。

方法

本研究纳入 82 例骨折正常愈合患者和 90 例骨折延迟愈合患者。采用 RT-qPCR 检测 LINC00339、miR-16-5p 和成骨标志物相关 mRNAs 的水平。采用 ROC 曲线分析验证 LINC00339 对骨折延迟愈合的预测潜力。采用双荧光素酶报告实验和 RIP 实验验证 LINC00339 与 miR-16-5p 的相互作用。采用 CCK-8 检测细胞增殖，采用流式细胞术检测细胞凋亡率。

结果

LINC00339 在骨折延迟愈合患者中显著上调，对该病具有较强的预测能力。过表达 LINC00339 抑制成骨细胞增殖，促进细胞凋亡，降低成骨标志物的 mRNA 水平（P<0.05）。miR-16-5p 被鉴定为 LINC00339 的靶 mRNA，LINC00339 对 miR-16-5p 发挥负向调控作用，而过表达 miR-16-5p 则减轻了 LINC00339 对骨折愈合的抑制作用（P<0.05）。

结论

本研究表明 LINC00339 可能作为骨折延迟愈合的诊断标志物，通过调节成骨细胞，揭示了 LINC00339/miR-16-5p 轴在骨折愈合中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb5/11348643/b7d91c4602b9/13018_2024_4998_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb5/11348643/6826abe6e3ad/13018_2024_4998_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb5/11348643/c309299a769e/13018_2024_4998_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb5/11348643/9d6989c6af1f/13018_2024_4998_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb5/11348643/b7d91c4602b9/13018_2024_4998_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb5/11348643/6826abe6e3ad/13018_2024_4998_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb5/11348643/c309299a769e/13018_2024_4998_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb5/11348643/9d6989c6af1f/13018_2024_4998_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cdb5/11348643/b7d91c4602b9/13018_2024_4998_Fig4_HTML.jpg

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