Long noncoding RNA endogenous bornavirus-like nucleoprotein acts as an oncogene by regulating microRNA-655-3p expression in T-cell acute lymphoblastic leukemia

Acute lymphocytic leukemia (ALL) is the most common malignant tumor in children with T-cell ALL (T-ALL), accounting for approximately 15% of all cases. Long noncoding RNAs (lncRNAs) are involved in the pathogenesis and progression of T-ALL. The present study aimed to explore the role and mechanism of action of lncRNA EBLN3P in T-ALL. We used quantitative reverse transcription-PCR (qRT-PCR) to determine the expression of lncRNA endogenous bornavirus-like nucleoprotein (EBLN3P), microRNA (miR)-655-3p, and the transcription level of matrix metalloproteinase-9 (MMP-9), and Western blot assay to quantify the protein expression level of cleaved-caspase3, caspase3, proliferating cell nuclear antigen (PCNA), and MMP-9. The potential binding sites between lncRNA EBLN3P and miR-655-3p were predicted using StarBase, and the interaction was further verified by dual-luciferase reporter assay and RNA pull-down assay. The proliferation ability of Jurkat cells was detected using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay, and their invasion and migration ability using transwell assay. Cell apoptosis was determined using flow cytometry (FCM) assay. The expression of lncRNA EBLN3P was upregulated while that of miR-655-3p was downregulated in human T-ALL cell lines and lncRNA EBLN3P negatively regulated miR-655-3p. LncRNA EBLN3P knockdown significantly inhibited proliferation, invasion, and migration of Jurkat cells and induced their apoptosis. Downregulating miR-655-3p reversed the effects of lncRNA EBLN3P knockdown on Jurkat cells. In conclusion, we confirmed for the first time that lncRNA EBLN3P is dysregulated in T-ALL cell lines, and lncRNA EBLN3P knockdown inhibited the malignant biological behaviors of T-ALL cells by up-regulating miR-655-3p.