Abstract
Diffuse large B cell lymphoma (DLBCL) is the most common non-Hodgkin lymphoma (NHL) globally, featuring heterogeneous clinical phenotypes and altered molecular manifestations. The long non-coding ribose nucleic acids (lncRNAs) play crucial roles in the diagnosis, treatment, and prognosis of DLBCL, requiring the exploration of complex functions and mechanisms. In this study, the expression of lncRNA TRIM52-AS1 in DLBCL tissues from the Cancer Genome Atlas (TCGA) database was initially analyzed and correlated to the data from collected clinical samples. Then, the significance of TRIM52-AS1 on the diagnosis and prognosis of DLBCL patients was predicted with the receiver-operating characteristic (ROC) curve and Kaplan-Meier (KM) analysis. Further, cell counting kit (CCK)-8, EdU staining, and flow cytometry analyses were performed to assess the effect of TRIM52-AS1 on DLBCL cell proliferation, apoptosis, and cell cycle. Then, the mechanism of TRIM52-AS1 sponging miR-577 to increase TRIM52 expression was explored using a starBase prediction approach, dual-luciferase reporter, RNA immunoprecipitation assay (RIPA), quantitative reverse transcription-polymerase chain reaction (RT-qPCR), and Western blot analyses. The experimental results confirmed the overexpression of TRIM52-AS1 in the DLBCL cell lines. Further, the high expression of TRIM52-AS1 predicted the poor Ann Arbor stage and were correlated with the presence of B symptoms, high international prognostic index, and poor disease prognosis. TRIM52-AS1 knockdown inhibited the DLBCL cell proliferation, and induced apoptosis and G0/G1 cycle arrest. Interestingly, the overexpression of TRIM52-AS1 increased the mRNA stability of TRIM52 through binding IGFBP3 protein and upregulated the TRIM52 protein expression by sponging miR-577. Together, the overexpressed TRIM52-AS1 could promote the DLBCL progression through IGFBP3/miR-218-5p/TRIM52 axis, highlighting the clinical significance of TRIM52-AS1 in the DLBCL diagnosis.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
