Abstract
Long-chain non-coding RNAs (LncRNAs) are expressed in diffuse large B-cell lymphoma (DLBCL) tissues and have played a regulatory role in DLBCL with a cancer-promoting effect. In this study, the role of LncRNA SNHG8 in the regulation of DLBCL cells is investigated, and its underlying mechanism is explored. The database of the Gene Expression Profiling Interactive Analysis (GEPIA) was searched, and the expression of SNHG8 in DLBCL and normal tissues was examined. The expression of SNHG8 was evaluated in several DLBCL cell lines and a normal lymphocyte cell line. It was found that SNHG8 was overexpressed in DLBCL tissues and cells in comparison with their normal counterparts. The short hairpin RNA (shRNA) plasmids of SNHG8 were transfected into DLBCL cells to knockdown the expression of SNHG8, followed by assays of proliferation, colony formation, apoptosis, and related protein expression. The results showed that the knockdown of SNHG8 significantly inhibited DLBCL cell proliferation and colony formation while promoting cell apoptosis. Moreover, the knockdown of SNHG8 reduced the expression of Ki-67, proliferating cell nuclear antigen (PCNA), and Bcl-2 and enhanced the expression of Bax and cleaved caspase 3/9. MiR-335-5p was predicted to be a potential target of SNHG8 by using the bioinformatics analysis, and the interaction between the two was validated by using the dual luciferase assay. In addition, the knockdown of SNHG8 increased the level of miR-335-5p, whereas miR-335-5p mimic decreased the expression of SNHG8. Finally, U2932 cells were co-transfected with or without sh-SNHG8 and miR-335-5p inhibitors, whose proliferation, colony formation, and apoptosis were determined subsequently. It was demonstrated that the presence of an miR-335-5p inhibitor partially canceled the inhibitory effects of the knockdown of SNHG8 on DLBCL cell proliferation and colony formation and the stimulating effects of the knockdown of SNHG8 on cell apoptosis. Taken together, our study suggests that lncRNA SNHG8 exerts a cancer-promoting effect on DLBCL via targeting miR-335-5p.
Highlights
Being an aggressive malignant B-cell lymphoma, diffuse large Bcell lymphoma (DLBCL) is the most common subtype of nonHodgkin lymphoma (NHL)
The objective of this study is to investigate the role of lncRNA SNHG8 in diffuse large B-cell lymphoma (DLBCL) cells and uncover the potential mechanism
We searched the database of the Gene Expression Profiling Interactive Analysis (GEPIA) and found that SNHG8 was significantly upregulated in the tissues of patients with DLBCL in comparison with that of normal healthy individuals (Figure 1A)
Summary
Being an aggressive malignant B-cell lymphoma, diffuse large Bcell lymphoma (DLBCL) is the most common subtype of nonHodgkin lymphoma (NHL). DLBCL accounts for about 40% of newly diagnosed NHL cases in western countries [1]. The lesions of DLBCL occur mainly on the lymph nodes, and some of them are found in the gastrointestinal tract, bone, and the central nervous system [2]. The lymph nodes of patients with DLBCL enlarge rapidly at an early stage, and symptoms such as fever and night sweat can occur. With the progression of DLBCL, the lesions show aggressive growth, resulting in poor treatment outcome [3]. The advancement of medicine contributes to a great progress in the therapeutic approach for the treatment of DLBCL, up to 40% of patients die from a relapse [4]. The molecular mechanism of the pathogenesis of DLBCL remains unclear, which seriously hinders the management of DLBCL
Sign-in/Register to view highlights & summary 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.
