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

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Udgivet i:bioRxiv (Jan 22, 2025)
Hovedforfatter: Xiao, Lanlan
Andre forfattere: 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
Udgivet:
Cold Spring Harbor Laboratory Press
Fag:
Rheumatoid arthritis
Tumor suppressor genes
Pathogenesis
Glycosylation
Phosphorylation
Metabolomics
Angiogenesis
Acetylation
Nitration
Quality of life
Tumors
Transcriptomics
Lysine
Methylation
Proteomics
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Resumen: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
Fuente:Biological Science Database