{"title":"Exploring shared pathogenesis of multiple myeloma and osteoporosis via bioinformatic analysis.","authors":"Yajie Wang, Chengdi Liu, Kegong Tang, Jiyun Zhang, Xinran Liu, Yiming Ma, Xiaofei Li","doi":"10.1080/17474086.2025.2465456","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>The purpose of this study is to explore the common differentially expressed genes (DEGs) between multiple myeloma (MM) and osteoporosis and the associated molecular mechanisms.</p><p><strong>Research design and methods: </strong>We obtained the overlapping DEGs between MM and osteoporosis with the GEO2R online tool. Then, the DEGs were clustered on the MetaCore website to identify the biological process and pathway. In addition, the STRING database and Cytoscape were used to construct the protein-protein interaction (PPI) network and identify hub genes. Finally, miRNA-gene and transcriptional factor (TF)-gene interaction networks were constructed.</p><p><strong>Results: </strong>A total of 252 genes were identified as DEGs in the overlapping two datasets. Functional analysis emphasizes the crucial role of the cell cycle in these two diseases. 10 hub genes were identified using cytoHubba, including CCNA2, ASPM, MKI67, FN1, FEN1, STAT1, DEPDC1, ITGB8, DYNC2LI1, HBEGF. In addition, according to the miRNA-gene and TF-gene interaction networks, part of TFs (RELA, TP53), and miRNAs (miR-26b-5p, miR-192-5p) may be identified as key regulators in MM and osteoporosis at the same time.</p><p><strong>Conclusions: </strong>The present study reveals the common pathogenesis of MM and osteoporosis. These shared pathways may provide new targets for further mechanistic studies of the pathogenesis and treatment of MM and osteoporosis.</p>","PeriodicalId":12325,"journal":{"name":"Expert Review of Hematology","volume":" ","pages":"167-176"},"PeriodicalIF":2.3000,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Expert Review of Hematology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/17474086.2025.2465456","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/2/14 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"HEMATOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: The purpose of this study is to explore the common differentially expressed genes (DEGs) between multiple myeloma (MM) and osteoporosis and the associated molecular mechanisms.
Research design and methods: We obtained the overlapping DEGs between MM and osteoporosis with the GEO2R online tool. Then, the DEGs were clustered on the MetaCore website to identify the biological process and pathway. In addition, the STRING database and Cytoscape were used to construct the protein-protein interaction (PPI) network and identify hub genes. Finally, miRNA-gene and transcriptional factor (TF)-gene interaction networks were constructed.
Results: A total of 252 genes were identified as DEGs in the overlapping two datasets. Functional analysis emphasizes the crucial role of the cell cycle in these two diseases. 10 hub genes were identified using cytoHubba, including CCNA2, ASPM, MKI67, FN1, FEN1, STAT1, DEPDC1, ITGB8, DYNC2LI1, HBEGF. In addition, according to the miRNA-gene and TF-gene interaction networks, part of TFs (RELA, TP53), and miRNAs (miR-26b-5p, miR-192-5p) may be identified as key regulators in MM and osteoporosis at the same time.
Conclusions: The present study reveals the common pathogenesis of MM and osteoporosis. These shared pathways may provide new targets for further mechanistic studies of the pathogenesis and treatment of MM and osteoporosis.
期刊介绍:
Advanced molecular research techniques have transformed hematology in recent years. With improved understanding of hematologic diseases, we now have the opportunity to research and evaluate new biological therapies, new drugs and drug combinations, new treatment schedules and novel approaches including stem cell transplantation. We can also expect proteomics, molecular genetics and biomarker research to facilitate new diagnostic approaches and the identification of appropriate therapies. Further advances in our knowledge regarding the formation and function of blood cells and blood-forming tissues should ensue, and it will be a major challenge for hematologists to adopt these new paradigms and develop integrated strategies to define the best possible patient care. Expert Review of Hematology (1747-4086) puts these advances in context and explores how they will translate directly into clinical practice.