BackgroundCircular RNAs (circRNAs) have been implicated in developing gastric cancer (GC). However, the role of circMRPL35 in GC remains unknown.MethodsThis study identified differentially expressed circMRPL35 using gene expression profiles GSE78092, GSE131414, and GSE100170. RNA R enzyme and RNA FISH assays were used to explore the origin, cyclization site, and cellular localization of circMRPL35. The functions of circMRPL35, miR-6809-3p, and ZNF90 in GC cells were evaluated through loss- and gain-of-function experiments. The epithelial-mesenchymal transition (EMT) process and the TGF-β1/SMAD signaling pathway were analyzed using Western blot and immunofluorescence assays. Subcutaneous tumor models in nude mice were utilized to evaluate the impact of circMRPL35 on GC cells. The interactions among circMRPL35, miR-6809-3p, and ZNF90 were confirmed through luciferase reporter and rescue assays.ResultsThe study demonstrated that circMRPL35, present in the cytoplasm and nucleus of MGC-803 and HGC-27 cells, originates from the cyclization of exons 4 and 5 on chromosome 2. In GC tissues and cells, circMRPL35 and ZNF90 were upregulated, while miR-6809-3p was downregulated. circMRPL35 and ZNF90 enhanced cell mobility and invasion and suppressed apoptosis by modulating the EMT process and TGF-β1/SMAD2/3 signaling pathway; conversely, miR-6809-3p exhibited the opposite effects. Mechanistically, circMRPL35 sponges miR-6809-3p to regulate ZNF90, thereby enhancing the phenotype of GC cells.ConclusionsThese results indicate that circMRPL35 acts as an oncogenic driver via the miR-6809-3p/ZNF90 axis, affecting the EMT process and the TGF-β1/SMAD2/3 signaling pathway to promote GC progression.

B-cell acute lymphoblastic leukemia (B-ALL) manifests as an abnormal proliferation of neoplastic B-cell lymphocytes, adversely affecting both children and adults. Despite the advancements in cancer research, B-ALL cure remains challenging due to the complexity of the disease and immense subtype heterogeneity. Better understanding of the molecular mechanisms driving B-ALL pathogenesis is imperative to identify the novel therapeutic markers that can impede disease progression. Genomic and transcriptomic studies involving patient samples have underscored the emerging role of long non-coding RNAs (lncRNAs) in the diverse B-ALL landscape. Their dysregulation has been linked to malignant proliferation, metastasis, and varying patient survival outcomes. Gaining detailed mechanistic insights into the role of lncRNAs in B-ALL pathophysiology is pivotal for understanding their contributions to disease progression and developing new therapeutics. Herein, we have comprehensively discussed B-ALL and its diverse subtypes, focusing on the pivotal role played by various lncRNAs in fine-tuning signaling pathways, disease heterogeneity and progression. We have also explored recent advances in our understanding of the diverse classes of lncRNA inhibitors, evaluating their potential as B-ALL therapeutics and challenges associated with their development.

Accurately identifying and quantifying human blood circular RNAs (circRNAs) from RNA-seq data is a critical bioinformatics challenge in biomarker discovery for human diseases. In this study, we present AQUARIUM-HB, a comprehensive bioinformatics pipeline for identifying, quantifying, annotating, and analyzing circRNAs from human blood transcriptomes. AQUARIUM-HB includes three functional modules. First, it identifies and annotates circRNAs from rRNA-depleted RNA-seq datasets of human blood samples. Second, it performs an in-depth expression analysis of blood circRNAs. Third, it constructs a reference set of full-length blood circRNAs. We demonstrate the application of AQUARIUM-HB using a human blood RNA-seq dataset from COVID-19 patients, showcasing its potential for improving the accuracy and depth of circRNA biomarker discovery.