Long Non-Coding RNA Paternally Expressed Imprinted Gene 10 (PEG10) Elevates Diffuse Large B-Cell Lymphoma Progression by Regulating Kinesin Family Member 2A (KIF2A) via Targeting MiR-101-3p
Jin Zhao, Liping Su, Jianjun Jiang
Department of Hematology, Affiliated Shanxi Tumor Hospital of Shanxi Medical University, Taiyuan, Shanxi, China (mainland)
Med Sci Monit 2020; 26:e922810
Available online: 2020-08-05
Diffuse large B-cell lymphoma (DLBCL) is a common malignant tumor in the immune system with high mortality. We investigated the functional effects of long non-coding RNA paternally expressed imprinted gene 10 (PEG10) on DLBCL progression.
MATERIAL AND METHODS: Real-time quantitative polymerase chain reaction was used to measure the level of PEG10, kinesin family member 2A (KIF2A) and microRNA-101-3p (miR-101-3p) in DLBCL tissues and cell lines. The relative protein level was detected by western blot analysis. The biological behaviors including cell proliferation, apoptosis, migration, and invasion were determined by MTT assay, flow cytometry analysis, and Transwell assays, respectively. Bioinformatics analysis and dual-luciferase reporter assay were performed to evaluate the interaction among PEG10, miR-101-3p, and KIF2A.
RESULTS: PEG10 and KIF2A level were significantly upregulated, while miR-101-3p was downregulated in DLBCL tissues and cells. PEG10 positively regulated KIF2A level in DLBCL. PEG10, or KIF2A deletion significantly inhibited the proliferative, migratory, and invasive abilities of DLBCL cells and elevated cell apoptosis in DLBCL cells. KIF2A upregulation partially reversed the effects of PEG10 downregulation on cell growth, metastasis, and apoptosis in DLBCL. Moreover, PEG10 negatively regulated miR-101-3p level and miR-101-3p upregulation exerted inhibition effects on the progression of DLBCL. Besides, miR-101-3p was a target of PEG10 and miR-101-3p could directly target KIF2A. PEG10 promoted KIF2A level by sponging miR-101-3p.
CONCLUSIONS: Our findings revealed that PEG10 played an oncogenic role in DLBCL progression, which might be a potential target for the treatment of DLBCL.
Keywords: Cell Proliferation, Lymphoma, B-Cell, MicroRNAs