Super-omics and PCAS reveal rheumatoid arthritis as a tumor-like disease

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Dades bibliogràfiques
Publicat a:	bioRxiv (Jan 22, 2025)
Autor principal:	Xiao, Lanlan
Altres autors:	Aishan, Nadire, Ju, Siwei, Zhao, Fengchao, Ouyang, Xiaoxi, Chen, Dazhi, Chen, Weiqian, Xie, Jie, Zhu, Danhua, Zhang, Junchi, Sun, Lingyun, Li, Yimin, Zhou, Dan, Hu, Qingqing, Wu, Jinzhi, Meng, Qingna, Zhou, Jichun, Xu, Danyi, Yu, Jingyi, Liang, Junyu, Cai, Yangjun, Zhang, Minmin, He, Yanlin, Sun, Zeyu, Wang, Linbo, Lin, Jin, Ji, Feiyang
Publicat:	Cold Spring Harbor Laboratory Press
Matèries:	Rheumatoid arthritis Tumor suppressor genes Pathogenesis Glycosylation Phosphorylation Metabolomics Angiogenesis Acetylation Nitration Quality of life Tumors Transcriptomics Lysine Methylation Proteomics
Accés en línia:	Citation/Abstract Full text outside of ProQuest
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Descripció
Resum:	Rheumatoid arthritis (RA) is a debilitating systemic autoimmune disorder that significantly impairs quality of life. To elucidate the molecular alterations in RA progression, we performed comprehensive super-omics analyses on synovial tissues from patients with joint trauma, arthritis, and RA. These analyses included transcriptomics, proteomics, metabolomics, microbiomics, and fourteen PTMs (phosphorylation, acetylation, lactylation, O-GlcNAc glycosylation, arginine monomethylation, lysine monomethylation, lysine dimethylation, lysine trimethylation, succinylation, malonylation, glutarylation, tyrosine nitration, N-glycosylation, and O-glycosylation). Additionally, we developed a protein-centered association study (PCAS) method to integrate these complex datasets. Using this approach, we identified key proteins, such as STK17B, and its interactors, which may be crucial in RA pathogenesis. Tumor-like features, including aberrant angiogenesis and epithelial-mesenchymal transition, were observed in RA, alongside the potential involvement of oncogenes and tumor suppressor genes. Finally, we constructed a molecular interaction blueprint of RA, providing a comprehensive framework for advancing RA pathogenesis, diagnosis, and therapy.Competing Interest StatementThe authors have declared no competing interest.
ISSN:	2692-8205
DOI:	10.1101/2025.01.17.633562
Font:	Biological Science Database