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Xing Liu,1 Guoqiang Zhong,2 Wenbin Li,1 Yiqian Zeng,3 Mingxing Wu1 1Department of Cardiology, Xiangtan Central Hospital, Xiangtan, Hunan, People’s Republic of China; 2Department of Cardiology, Guangxi Cardiovascular Institute, The First Affiliated Hospital of Guangxi Medical University, Guangxi, People’s Republic of China; 3Department of Critical Care Medicine, Zhuzhou Central Hospital, Zhuzhou, Hunan, People’s Republic of ChinaCorrespondence: Yiqian ZengDepartment of Critical Care Medicine, Zhuzhou Central Hospital, Zhuzhou, Hunan, People’s Republic of ChinaEmail zengyiqian@stu.gxmu.edu.cnMingxing WuDepartment of Cardiology, Xiangtan Central Hospital, Xiangtan, Hunan, People’s Republic of China Email wmx917121@126.comBackground: At present, the mechanisms behind atrial fibrillation (AF) pathogenesis are still unclear. We construct a ceRNA immunoregulatory network to further understand the mechanism of AF.Methods: Four AF mRNA datasets from the Gene Expression Omnibus (GEO) database were integrated by SVA method. AF-related immune genes (AF-IRGs) were selected via combining ImmPort database with the genes in the module most associated with AF obtained by a weighted gene coexpression network analysis (WGCNA). Then, circRNA and miRNA expressions from the GEO database were extracted and mapped with related databases. Next, an immune-related circRNA-miRNA-mRNA ceRNA network was constructed and hub genes were filtered from a protein–protein interaction (PPI) network, and the differentially expressed (DE) hub genes in AF were further screened. Additionally, immune infiltration was investigated in AF by using CIBERSORT. Subsequently, the relationships between DE hub genes and AF-related infiltrating immune cells were performed by using Pearson correlation coefficients. Ulteriorly, the immune-cells-related ceRNA subnetwork in AF was built.Results: A total of 95 AF-IRGs were detected, and an immune-related ceRNA network in AF was constructed with 12 circRNAs, 7 miRNAs and 50 mRNAs. The immune infiltration analysis indicated that a higher level of neutrophils, as well as a lower level of T cells regulatory (Tregs) and NK cells activated in AF. Four DE hub genes (CXCL12, IL7R, TNFSF13B, CD8A) were associated with Tregs or NK cells activated immune cells (P < 0.05). Tregs or NK cells activated immune cells-related ceRNA subnetwork including 5 circRNAs (has_circ_0001190, has_circ_0006725, has_circ_0079284, has_circ_0005299, and has_circ_0002103), 4 miRNAs (has-miR-198, has-miR-623, has-miR-1246, and has-miR-339-3p) and 4 DE hub genes was eventually constructed in AF.Conclusion: Our results provide new insights into the molecular mechanisms governing AF progression from the perspective of immune-related ceRNA network.Keywords: atrial fibrillation, competitive endogenous RNA, immune infiltration

The long non-coding RNA (lncRNA), urothelial carcinoma-associated 1 (UCA1), belongs to cancer-related lncRNAs implicated in various carcinomas, including colorectal and gastric cancers. Nonetheless, the role and underlying mechanisms of UCA1 in retinoblastoma are still unclear. This study found that UCA1 expression in retinoblastoma tissues and cells was dramatically upregulated relative to that of healthy controls. Functionally, UCA1 knockdown could suppress retinoblastoma cells’ proliferation, migration and invasion, and facilitate their apoptosis. Knockdown of UCA1 also retarded the growth of xenograft tumors in vivo. Mechanistically, UCA1 promoted c-myc expression through sponging miR-124. miR-124 inhibition or c-myc overexpression partially reversed the effects of UCA1 knockdown on retinoblastoma cells. Overall, lncRNA UCA1 may exert an oncogenic effect on retinoblastoma progression through the miR-124/c-myc axis, which might serve as a promising retinoblastoma treatment target.