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铁死亡相关基因的综合分析揭示骨质疏松症患者的潜在治疗靶点：一项计算分析和实验

Comprehensive analysis of ferroptosis-related genes reveals potential therapeutic targets in osteoporosis patients: a computational analysis and experiments.

作者信息

Chen Sihui, Jiang Yi, Xie Guoqin, Wu Peng, Zhu Jinyu

机构信息

Department of Orthopedics, First Hospital of Jiaxing, Jiaxing, China.

College of Medicine, Jiaxing University, Jiaxing, China.

出版信息

Front Genet. 2025 Jan 10;15:1522809. doi: 10.3389/fgene.2024.1522809. eCollection 2024.

DOI:10.3389/fgene.2024.1522809
PMID:39867575
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11757248/
Abstract

BACKGROUND

Ferroptosis-related genes have been reported to play important roles in many diseases, but their molecular mechanisms in osteoporosis have not been elucidated.

METHODS

Based on two independent GEO datasets (GSE35956 and GSE35958), and GSE35959 as the validation dataset, we comprehensively elucidated the pathological mechanism of ferroptosis-related genes in osteoporosis by GO analyses, KEGG analyses and a PPI network. Then, We used Western Blot (WB) and Quantitative real-time polymerase chain reaction (qPCR) to verify the expression level of KMT2D, a ferroptosis-related hub gene, in clinical samples. Subsequently, we predicted the upstream miRNA of KMT2D gene and analyzed the mechanism of KMT2D in osteoporosis, the potential prognostic value and its immune invasion of KMT2D in pan-cancer.

RESULTS

This study identified KMT2D and MYCN, TP63, RELA, SOX2, and CDKN1A as key ferroptosis-related genes in osteoporotic cell aging. The independent dataset validated that the expression level of KMT2D was significantly upregulated in osteoporosis samples. The experimental verification results of qPCR and WB indicate that KMT2D is highly expressed in patients with osteoporosis. Further analysis revealed that the hsa-miR-204-5p-KMT2D axis may play an important role in the aging of osteoporotic cells. The analysis of KMT2D reveals that KMT2D may mainly play a role in the aging of osteoporotic cells through epigenetics and the value in pan-cancer.

CONCLUSION

The study provides a theoretical basis for the treatment of osteoporosis.

摘要

背景

据报道，铁死亡相关基因在多种疾病中发挥重要作用，但其在骨质疏松症中的分子机制尚未阐明。

方法

基于两个独立的GEO数据集（GSE35956和GSE35958），并将GSE35959作为验证数据集，我们通过基因本体（GO）分析、京都基因与基因组百科全书（KEGG）分析和蛋白质-蛋白质相互作用（PPI）网络全面阐明了铁死亡相关基因在骨质疏松症中的病理机制。然后，我们使用蛋白质免疫印迹法（WB）和定量实时聚合酶链反应（qPCR）来验证临床样本中铁死亡相关枢纽基因KMT2D的表达水平。随后，我们预测了KMT2D基因的上游微小RNA（miRNA），并分析了KMT2D在骨质疏松症中的作用机制、其在泛癌中的潜在预后价值及其免疫浸润情况。

结果

本研究确定KMT2D以及MYCN、TP63、RELA、SOX2和CDKN1A为骨质疏松细胞衰老中关键的铁死亡相关基因。独立数据集验证了骨质疏松症样本中KMT2D的表达水平显著上调。qPCR和WB的实验验证结果表明，KMT2D在骨质疏松症患者中高表达。进一步分析表明，hsa-miR-204-5p-KMT2D轴可能在骨质疏松细胞衰老中起重要作用。对KMT2D的分析表明，KMT2D可能主要通过表观遗传学在骨质疏松细胞衰老中发挥作用以及在泛癌中的价值。

结论

该研究为骨质疏松症的治疗提供了理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/292b/11757248/21667ca368ec/fgene-15-1522809-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/292b/11757248/21667ca368ec/fgene-15-1522809-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/292b/11757248/7ed79f61cdc9/fgene-15-1522809-g005.jpg
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