Upregulated miR-96-5p inhibits cell proliferation by targeting HBEGF in T-cell acute lymphoblastic leukemia cell line

被引:3
|
作者
Xu, Kaihong [1 ]
Yan, Xiao [1 ]
Ouyang, Guifang [1 ]
Feng, Jinyi [2 ]
Ye, Lilin [2 ]
Hu, Xuezhen [3 ,4 ]
Liu, Dingsheng [2 ]
机构
[1] Ningbo First Hosp, Dept Hematol, Ningbo 315000, Zhejiang, Peoples R China
[2] Shanghai Univ Med & Hlth Sci, Affiliated Zhoupu Hosp, Dept Oncol & Hematol, 1500 Zhouyuan Rd, Shanghai 201318, Peoples R China
[3] Wenzhou Med Univ, Affiliated Hosp 2, Dept Emergency Med, Wenzhou City 325000, Zhejiang, Peoples R China
[4] Wenzhou Med Univ, Yuying Childrens Hosp, Wenzhou City 325000, Zhejiang, Peoples R China
关键词
miR-96-5p; T-cell acute lymphoblastic leukemia; Jurkat T cells; HBEGF; CANCER;
D O I
10.5603/FHC.a2020.0018
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Introduction. microRNAs (miRNAs) are critical for tumorigenesis and progression of T-cell acute lymphoblastic leukemia (T-ALL). MiR-96-5p has been shown to play important roles in the development of many cancers, but its roles in T-ALL have yet not been studied. Materials and methods. miR-96-5p expression was detected in T-leukemic cells from peripheral blood of 30 patients with T-ALL using real-time quantitative PCR (RT-qPCR). TargetScan database was utilized to identify the target genes for miR-96-5p, and their target relationship was verified by western blot, dual luciferase reporter assay and RT-qPCR. The effects of miR-96-5p on the viability and proliferation of T-leukemic cells (Jurkat cells) were respectively determined using MTT and BrdU incorporation assays. Results. miR-96-5p presented low expression levels by qPCR in peripheral blood of T-ALL patients compared to healthy volunteers. Upregulated miR-96-5p by miR-96-5p mimic transfection markedly inhibited the viability and proliferation of Jurkat cells. Furthermore, miR-96-5p negatively regulated the expression of its target gene, HBEGF. The decreased viability and proliferation of Jurkat cells caused by miR-96-5p over-expression was suppressed after the introduction of HBEGF plasmid. Conclusions. The presented study showed that upregulation of miR-96-5p inhibited the viability and proliferation of Jurkat T-leukemic cells through suppressing HBEGF expression. Our study provides a novel sight for understanding the pathological mechanism of T-ALL and suggests that miR-96-5p may be a potential biomarker for the therapy and diagnosis of T-ALL.
引用
收藏
页码:219 / 226
页数:8
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