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Additional file 1: Figure S1. Mutation Analysis of the bladder cancer cohort.Oncoplot of the 44 UBC samples..Top 10 mutated genes in the UBC cohorts.. Top 10 pathways that were affected by the mutations in this UBC cohort.. Co-barplot with TCGA bladder cancer dataset showed the mutation frequency of the driver genes of the bladder cancers.. Variant allele frequency of the driver genes of the bladder cancer samples. Numbers in the first line represent the mutation hits in each gene in this cohort. Figure S2. Differential expression analysis between bladder cancer and paracancerous samples.Volcano plot for differentially expressed genes in bladder cancer samples.Pathway enrichment analysis of up-regulated and down-regulated genes in bladder cancer samples. Figure S3. Differential expression analysis between recurrent and primary bladder cancer samples.Volcano plot for differentially expressed genes in recurrent bladder cancer samples.Pathway enrichment analysis of up-regulated and down-regulated genes in recurrent bladder cancer samples. Figure S4. Pathway enrichment of 5mC and 5hmC DMRs in recurrent bladder cancer samples. Figure S5. Track plots of 5hmC DMRs annotated to fatty acid metabolism genes in recurrent bladder cancer samples. Figure S6. PD-L1 expression level in PD-L1 high and PD-L1 low UBC samples. Figure S7. Differential expression analysis between PD-L1-high and -low bladder cancer samples.Volcano plot for differentially expressed genes in PD-L1-high bladder cancer samples.Pathway enrichment analysis of up-regulated in PD-L1-high bladder cancer samples. Figure S8. Pathway enrichment of 5mC and 5hmC DMRs in PD-L1-high bladder cancer samples. Figure S9. Pathway enrichment of 5mC hypo DMRs and 5hmC hypo DMRs that are associated with significant DEGs in PD-L1 highly expressed bladder cancer. Figure S10. Driver mutations in recurrent and PD-L1 overexpression UBC samples.Please check if the additional files are captured and presented correctly.We confirmed that additional files are captured and presented correctly.As per journal requirements, every additional file must have a corresponding caption. In this regard, please be informed that the caption was taken from the additional e-file itself. Please advise if the action taken is appropriate and amend if necessary.We confirmed that this action is correct and no futher amend is necessary.

Background: With the continued advancement of RNA-seq (RNA-sequencing), microRNA (miRNA) editing events have been demonstrated to play an important role in different malignancies. However, there is yet no description of the miRNA editing events in recurrent bladder cancer.Objective: To identify and compare miRNA editing events in primary and recurrent bladder cancer, as well as to investigate the potential molecular mechanism and its impact on patient prognosis.Methods: We examined the mRNA and miRNA transcriptomes of 12 recurrent bladder cancer cases and 13 primary bladder cancer cases. The differentially expressed mRNA sequences were analyzed. Furthermore, we identified the differentially expressed genes (DEGs) in recurrent bladder cancer. The Gene Ontology (GO) functional enrichment analyses on DEGs and gene set enrichment analysis were performed. The consensus molecular subtype (CMS) classification of bladder cancer was identified using the Consensus MIBC package in R (4.1.0); miRNA sequences were then further subjected to differentially expressed analysis and pathway enrichment analysis. MiRNA editing events were identified using miRge3.0. miRDB and TargetScanHuman were used to predict the downstream targets of specific differentially edited or expressed miRNAs. The expression levels of miR-154-5p and ADAR were validated by RT-qPCR. Finally, survival and co-expression studies were performed on the TCGA-BLCA cohort.Results: First, the mRNA expression levels in recurrent bladder cancer changed significantly, supporting progression via related molecular signal pathways. Second, significantly altered miRNAs in recurrent bladder cancer were identified, with miR-154-5p showing the highest level of editing in recurrent bladder cancer and may up-regulate the expression levels of downstream targets HS3ST3A1, AQP9, MYLK, and RAB23. The survival analysis results of TCGA data revealed that highly expressed HS3ST3A1 and RAB23 exhibited poor prognosis. In addition, miR-154 editing events were found to be significant to CMS classification.Conclusion: MiRNA editing in recurrent bladder cancer was detected and linked with poor patient prognosis, providing a reference for further uncovering the intricate molecular mechanism in recurrent bladder cancer. Therefore, inhibiting A-to-I editing of miRNA may be a viable target for bladder cancer treatment, allowing current treatment choices to be expanded and individualized.

Cancer is a major public health problem worldwide. Studies on oncogenes and tumor-targeted therapies have become an important part of cancer treatment development. In this review, we summarize and systematically introduce the gene enhancer of rudimentary homolog (ERH), which encodes a highly conserved small molecule protein. ERH mainly exists as a protein partner in human cells. It is involved in pyrimidine metabolism and protein complexes, acts as a transcriptional repressor, and participates in cell cycle regulation. Moreover, it is involved in DNA damage repair, mRNA splicing, the process of microRNA hairpins as well as erythroid differentiation. There are many related studies on the role of ERH in cancer cells; however, there are none on tumor-targeted therapeutic drugs or related therapies based on the expression of ERH. This study will provide possible directions for oncologists to further their research studies in this field.

Additional file 1.

Additional file 1.