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

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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
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Cold Spring Harbor Laboratory Press
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LEADER 00000nab a2200000uu 4500
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022 |a 2692-8205 
024 7 |a 10.1101/2025.01.17.633562  |2 doi 
035 |a 3158241600 
045 0 |b d20250122 
100 1 |a Xiao, Lanlan 
245 1 |a Super-omics and PCAS reveal rheumatoid arthritis as a tumor-like disease 
260 |b Cold Spring Harbor Laboratory Press  |c Jan 22, 2025 
513 |a Working Paper 
520 3 |a 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. 
653 |a Rheumatoid arthritis 
653 |a Tumor suppressor genes 
653 |a Pathogenesis 
653 |a Glycosylation 
653 |a Phosphorylation 
653 |a Metabolomics 
653 |a Angiogenesis 
653 |a Acetylation 
653 |a Nitration 
653 |a Quality of life 
653 |a Tumors 
653 |a Transcriptomics 
653 |a Lysine 
653 |a Methylation 
653 |a Proteomics 
700 1 |a Aishan, Nadire 
700 1 |a Ju, Siwei 
700 1 |a Zhao, Fengchao 
700 1 |a Ouyang, Xiaoxi 
700 1 |a Chen, Dazhi 
700 1 |a Chen, Weiqian 
700 1 |a Xie, Jie 
700 1 |a Zhu, Danhua 
700 1 |a Zhang, Junchi 
700 1 |a Sun, Lingyun 
700 1 |a Li, Yimin 
700 1 |a Zhou, Dan 
700 1 |a Hu, Qingqing 
700 1 |a Wu, Jinzhi 
700 1 |a Meng, Qingna 
700 1 |a Zhou, Jichun 
700 1 |a Xu, Danyi 
700 1 |a Yu, Jingyi 
700 1 |a Liang, Junyu 
700 1 |a Cai, Yangjun 
700 1 |a Zhang, Minmin 
700 1 |a He, Yanlin 
700 1 |a Sun, Zeyu 
700 1 |a Wang, Linbo 
700 1 |a Lin, Jin 
700 1 |a Ji, Feiyang 
773 0 |t bioRxiv  |g (Jan 22, 2025) 
786 0 |d ProQuest  |t Biological Science Database 
856 4 1 |3 Citation/Abstract  |u https://www.proquest.com/docview/3158241600/abstract/embedded/J7RWLIQ9I3C9JK51?source=fedsrch 
856 4 0 |3 Full text outside of ProQuest  |u https://www.biorxiv.org/content/10.1101/2025.01.17.633562v1