lncRNA PVT1对急性髓系白血病HL-60细胞增殖、凋亡的影响  被引量:1

Effects of lncRNA PVT1 interference on the proliferation and apoptosis of acute myeloid leukemia cells

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作  者:陈珊[1] 安和兵[1] 王腾飞 宗广帅 周蕾 CHEN Shan;AN Hebing;WANG Tengfei(Department of Laboratory Medicine,the Second Affiliated Hospital of Hebei North University,Hebei,Zhangjiakou 075100,China)

机构地区:[1]河北北方学院附属第二医院检验科,河北省张家口市075100

出  处:《河北医药》2024年第13期1936-1939,1945,共5页Hebei Medical Journal

基  金:河北省卫生健康委员会科研基金项目(编号:20200492)。

摘  要:目的 探讨长链非编码RNA PVT1基因(lncRNA PVT1)对人急性髓系白血病(AML)HL-60细胞增殖、凋亡的影响。方法 选取106例AML患者为试验组,同期健康体检志愿者100例为对照组,采用实时荧光定量聚合酶链反应(RT-qPCR)检测外周血lncRNA PVT1表达。以干扰lncRNA PVT1的质粒转染HL-60细胞株(si-lncRNA PVT1组),同时将转染空载体的HL-60细胞设为对照组(si-Control组),另设正常组。RT-qPCR技术检测细胞中lncRNA PVT1的表达;CCK-8检测细胞的增殖率;流式细胞术检测细胞周期和凋亡的变化;Western blot和RT-qPCR技术检测细胞中细胞周期相关蛋白D1(Cyclin D1)、细胞周期依赖性蛋白激酶抑制因子1A(P21)、B淋巴细胞瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)、天冬氨酸蛋白水解酶3 (Caspase 3)表达。结果 试验组患者lncRNA PVT1表达水平高于对照组(P<0.05)。干扰lncRNA表达后HL-60细胞中,si-lncRNA PVT1组lncRNA PVT1水平显著低于si-Control组(P<0.05)。si-lncRNA PVT1组细胞增殖率显著低于si-Control组(P<0.05)。敲低lncRNA PVT1后细胞被显著阻滞于G1期,且明显诱导细胞的凋亡(P<0.05)。si-lncRNA PVT1组与si-Control组比较,Cyclin D1、Bcl-2表达降低,P21、Bax、Caspase 3表达升高(P<0.05)。结论 敲低lncRNA PVT1可抑制HL-60细胞的增殖并诱导其凋亡,提示lncRNA PVT1可能作为AML防治的一个分子靶点。Objective To investigate the effect of long non-coding RNA plasmacytoma variant translocation 1(lncRNA PVT1)on the proliferation and apoptosis of the line human leukemia cell line(HL-60).Methods A total of 106 patients with acute myeloid leukemia(AML)were selected as the experimental group,and 100 healthy volunteers during the same period were selected as the control group.Real-time fluorescence quantitative polymerase chain reaction(RT-qPCR)was used to detect the plasma expression of lncRNA PVT1.HL-60 cells were treated with blank control,or transfected with si-l ncRNA PVT1 or si-Control.LncRNA PVT1 level was detected by RT-qPCR.Cell proliferative rate was measured by CCK-8 assay.Cell cycle progression and apoptosis were examined by flow cytometry.Expression levels of cell cycle related protein D1(Cyclin D1),cyclin-dependent kinase inhibitor 1A(P21),B-cell lymphoma-2(BCL-2),Bcl-2 related X protein(Bax),and aspartate proteolytic enzyme 3(Caspase 3)were detected by Western blot and RT-qPCR.Results Plasma lncRNA PVT1 was significantly higher in the experimental group than that of control group(P<0.05).Knockdown of lncRNA PVT1 significantly downregulated its level in HL-60 cells than those transfected with si-Control(P<0.05).Knockdown of lncRNA PVT1 significantly decreased cell proliferative rate,arrested cell cycle in G1 phase and induced apoptosis in HL-60 cells(P<0.05).Compared with those transfected with si-Control,transfection of si-lncRNA PVT1 significantly downregulated Cyclin D1 and Bcl-2,but upregulated P21,Bax and Caspase 3(P<0.05).Conclusion Knockdown of lncRNA PVT1 can inhibit the proliferation and induce apoptosis of HL-60 cells,suggesting that lncRNA PVT1 may serve as a molecular target for the prevention and treatment of AML.

关 键 词:急性白血病 lncRNA PVT1 增殖 凋亡 

分 类 号:R733.7[医药卫生—肿瘤]

 

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