This study aims to investigate the mechanism of the non-coding RNA starting in the 3' untranslated region of complement 5 (C5T1lncRNA) and its binding proteins in the pathogenesis of rheumatoid arthritis (RA). The RNA-protein interaction method was adopted to identify binding proteins of C5T1lncRNA and their functions were studied. MH7A human RA synovial fibroblast cell line was infected with lentivirus to establish a stable pcDNA3.1-C5T1lncRNA cell line. RNA pull-down assay and mass spectrometry analysis were used to identify the interacting proteins of C5T1lncRNA. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes  (KEGG) enrichment and protein-protein interaction network (PPI) analysis were used to screen for the key interacting proteins of C5T1lncRNA. Western blotting was used to verify the interactions between C5T1lncRNA and the key proteins. The results showed that 55 interacting proteins of C5T1lncRNA were identified, among which 3 key proteins were found, including the RNA binding motif protein X-linked (RBMX), the heterogeneous nuclear ribonucleoprotein H1 (HNRNPH1), and the DExD/H-box helicase 9 (DHX9). These proteins were mainly closely related to the tissue-specific regulation of gene transcription and the selective splicing of several precursor mRNAs. Western blotting confirmed the binding of RBMX to C5T1lncRNA. This study suggests that C5T1lncRNA may regulate gene expression by RNA splicing and processing modifications via RBMX interaction, thereby promoting the occurrence and development of RA.

 Myasthenia gravis (MG) is an autoimmune disease mediated by pathogenic autoantibodies targeting the neuromuscular junction. Traditional immunotherapies have limitations such as slow onset, variable efficacy, and long-term safety risk. In recent years, the application of targeted biologics has significantly advanced the precision-based transformation of MG treatment. Current breakthrough biologics primarily fall into two categories: complement inhibitors and neonatal Fc receptor (FcRn) antagonists. FcRn antagonists (e.g., efgartigimod, rozanolixizumab) rapidly reduce pathogenic antibody levels by blocking the IgG recycling pathway, leading to symptom improvement within days. Complement inhibitors (e.g., eculizumab, ravulizumab) precisely inhibit complement C5 activity, reducing the formation of membrane attack complexes (MAC) and protecting the structural integrity of the neuromuscular junction, making them particularly suitable for acetylcholine receptor (AChR) antibody-positive patients. Additionally, B cell depleting agents offer an effective option for certain refractory MG cases. Current challenges include long-term safety, treatment costs, and optimization of individualized strategies. Future directions will concentrate on targeted combination therapies, the development of novel drug delivery systems, and the exploration of biomarkers. In summary, biologics are driving the transformation of MG treatment towards precision and efficiency, with future efforts focusing on drug accessibility and individualization of clinical applications.

为探讨食管鳞状细胞癌(esophageal squamous cell carcinoma, ESCC)患者外周血小核仁RNA71B(small nucleolar RNA 71B, SNORA71B)表达水平及其与PDGL1的相关性,评估其作为无创生物标志物的潜力，选取48例ESCC患者作为ESCC组,并纳入30例健康志愿者作为正常对照组。采用qRT-PCR检测ESCC组和正常对照组外周血中SNORA71B的表达水平；MTS细胞增殖实验、划痕实验和Transwell实验分别检测过表达SNORA71B对ESCC细胞株增殖、迁移和侵袭的影响;蛋白免疫荧光染色检测SNORA71B对细胞上皮间质转化(epithelial-mesenchymal transition,EMT)相关蛋白的影响;转录组测序分析SNORA71B可能作用的靶点及信号通路；在外周血和ESCC细胞中检测SNORA71B对PDGL1的影响。结果显示,与正常对照组比较,SNORA71B在ESCC患者外周血中的表达水平显著升高( P<0.05);过表达SNORA71B后,ESCC细胞的增殖、迁移和侵袭能力显著增强(P<0.05)；转录组测序结果显示, SNORA71B与PDGL1和PDG1免疫检查点途径有关；ESCC细胞中敲低或过表达SNORA71B表达，PDGL1的蛋白表达随之降低或升高。该研究提示, SNORA71B在ESCC中可以促进肿瘤恶性生物学行为并调节PDGL1表达，其有可能成为评估ESCC新辅助治疗反应的潜在分子标志物。