OBJECTIVE: This study aimed to investigate the expression profiles of plasma exosomal RNAs in patients with Diffuse Large B-Cell Lymphoma (DLBCL) and evaluate their diagnostic potential. METHODS: Exosomes were isolated from 9 DLBCL patients and 9 healthy controls, followed by whole transcriptome RNA sequencing to identify differentially expressed RNAs. Key RNAs were selected and validated via qRT-PCR using an independent cohort of 41 treatment-naïve DLBCL patients and 41 healthy controls. The StarBase database was utilized to predict target relationships and construct lncRNA/miRNA competing endogenous RNA (ceRNA) pairs. Diagnostic efficacy was assessed using Receiver Operating Characteristic (ROC) curve analysis. RESULTS: High-throughput sequencing revealed significant RNA expression differences between DLBCL patients and healthy controls. Specifically, 35 microRNAs (miRNAs), 1604 long non-coding RNAs (lncRNAs), and 330 messenger RNAs (mRNAs) were differentially expressed in the DLBCL group, while no significant differences were observed in circular RNA (circRNA) expression. Two ceRNA pairs, MALAT1/hsa-miR-181a-5p and SLC9A3-AS1/hsa-miR-10a-5p, were constructed. qRT-PCR validation confirmed that hsa-miR-181a-5p and hsa-miR-10a-5p were significantly down-regulated, while SLC9A3-AS1 was up-regulated in the DLBCL group; MALAT1 expression showed no significant difference. ROC analysis demonstrated Area Under the Curve (AUC) values of 0.813 for hsa-miR-181a-5p, 0.800 for hsa-miR-10a-5p, and 0.787 for SLC9A3-AS1. The combined AUC for SLC9A3-AS1 and hsa-miR-10a-5p was 0.8226, and for SLC9A3-AS1 and hsa-miR-181a-5p was 0.852. CONCLUSION: Exosome-derived miRNAs, lncRNAs, and mRNAs exhibit distinct expression patterns in DLBCL patients compared to healthy controls. The RNAs hsa-miR-181a-5p, hsa-miR-10a-5p, and SLC9A3-AS1 show promise as diagnostic biomarkers for DLBCL, with combined RNA panels offering improved diagnostic efficacy over single markers. The SLC9A3-AS1/hsa-miR-10a-5p pair may form a regulatory network influencing DLBCL pathogenesis.
Ma et al. (Tue,) studied this question.