假基因来源的LncRNA SOD1P3、CCT8P1在急性髓性白血病中的表达及临床病理参数分析  

Expression of Pseudogene-derived LncRNA SOD1P3 and CCT8P1 and clinicopathological parameters in acute myeloid leukemia

作　　者：吴胜 王珏 沙钰 刘桦 夏楠 陈静 Wu Sheng;Wang Jue;Sha Yu;Liu Hua;Xia Nan;Chen Jing(Department of Pathology,Jing Jiang People’s Hospital Affiliated to Yangzhou University,Jing Jiang 214500,Jiangsu)

机构地区：[1]扬州大学附属靖江市人民医院病理科,江苏靖江214500

出　　处：《中国组织化学与细胞化学杂志》2024年第6期524-532,共9页Chinese Journal of Histochemistry and Cytochemistry

基　　金：靖江市人民医院院内科研项目(JRY-KY-2024-002)。

摘　　要：目的探讨假基因来源的LncRNA SOD1P3、CCT8P1在急性髓系白血病(acute myeloid leukemia,AML)中的表达及与患者临床病理特征的关系。方法收集2019年1月—2023年1月于本院就诊的132例AML患者骨髓样本进行研究,RT-qPCR实验检测骨髓样本中LncRNA SOD1P3、CCT8P1、ENO1P1表达;构建过表达LncRNA SOD1P3、CCT8P1、ENO1P1 AML移植瘤小鼠,检测小鼠肿瘤体积和重量;体外培养HL-60细胞,并随机分为对照组、NC组、SOD1P3组、CCT8P1组、ENO1P1组,根据组别名字将相应的质粒转染至细胞;分别检测各组细胞增殖、侵袭、凋亡和S期细胞比例;Western blot检测Raf/MEK/ERK通路蛋白表达。结果SOD1P3高表达与低表达样本在红细胞计数(RBC)与骨髓原始细胞比中存在差异,CCT8P1高表达与低表达样本在骨髓原始细胞比中存在差异;高表达SOD1P3或ENO1P1显著抑制小鼠瘤体生长,过表达CCT8P1显著促进小鼠瘤体生长;高表达SOD1P3可显著抑制HL-60细胞增殖、侵袭并诱导凋亡,高表达CCT8P1可显著促进细胞增殖和侵袭;高表达SOD1P3可显著抑制Raf、MEK、ERK蛋白磷酸化,高表达CCT8P1可显著上调Raf、MEK、ERK蛋白磷酸化。结论假基因来源的LncRNA SOD1P3、CCT8P1差异表达可通过影响细胞增殖、侵袭、凋亡及Raf/MEK/ERK信号通路参与AML发展,有望成为AML患者特异性肿瘤标志物。Objective To investigate the expression of pseudogene-derived LncRNA SOD1P3 and CCT8P1 in acute myeloid leukemia(AML)and their relationship with the clinicopathological features of patients.Methods Bone marrow samples of 132 AML patients admitted to our hospital from January 2019 to January 2023 were collected for study.The expression of Pseudogene-derived LncRNA SOD1P3,CCT8P1 and ENO1P1 in the bone marrow samples was detected by RT-qPCR.Construct overexpressed LncRNA SOD1P3,CCT8P1 and ENO1P1 AML transplanted tumor mice,tumor volume and weight were detected.HL-60 cells were cultured in vitro and randomly divided into control group,NC group,SOD1P3 group,CCT8P1 group and ENO1P1 group.The corresponding plasmid was transfected into the cells according to the group name.cell proliferation,invasion,apoptosis and the proportion of S-phase cells were detected;The expression of Raf/MEK/ERK pathway protein was detected by Western blot.Results There were differences in red blood cell count(RBC)and bone marrow original cell ratio between samples with high and low expression of SOD1P3;There were differences in the ratio of bone marrow original cells between the samples with high and low expression of CCT8P1;Overexpression of SOD1P3 or ENO1P1 significantly inhibited tumor weight and volume,and overexpression of CCT8P1 significantly promoted tumor growth(all P<0.01).High expression of SOD1P3 significantly inhibited the proliferation and invasion of HL-60 cells and induced apoptosis,while high expression of CCT8P1 significantly promoted the proliferation and invasion of HL-60 cells(all P<0.05).High expression of SOD1P3 significantly inhibited the protein phosphorylation of Raf,MEK and ERK,and high expression of CCT8P1 significantly up-regulated the protein phosphorylation of Raf,MEK and ERK(all P<0.05).Conclusion The differential expression of pseudogene-derived LncRNA SOD1P3 and CCT8P1 can participate in the development of AML by affecting cell proliferation,invasion,apoptosis and Raf/MEK/ERK signaling pathways,and pseudogene-d

关 键 词：急性髓系白血病 假基因 差异表达 病理参数 移植瘤 细胞增殖 侵袭 Raf/MEK/ERK通路 

分 类 号：R733.71[医药卫生—肿瘤]