摘要
目的研究长链非编码RNA linc00467在儿童急性髓系白血病(AML)中的表达及功能。方法采集2016年5月至2018年6月确诊的5例儿童AML病例的骨髓标本,以进行骨髓检查提示为正常的3例儿童骨髓标本作为对照。通过实时荧光定量PCR检测并比较linc00467在两组样本中的表达量。通过慢病毒系统在AML细胞(HL-60)中过表达linc00467(linc00467过表达组),以表达绿色荧光蛋白(GFP)的空载体转入AML细胞作为对照(GFP对照组);通过慢病毒系统将干扰序列插入AML细胞中(sh-linc00467干扰组),以插入随机序列作为对照(sh-NC对照组)。检测各组细胞增殖情况及对阿霉素耐药性的影响。结果与对照组儿童相比,linc00467在儿童AML中表达上调。过表达与干扰linc00467表达对细胞增殖无明显影响(P>0.05)。相比于GFP对照组,过表达linc00467在0.1、0.2、0.3、0.4、0.5μg/mL阿霉素浓度作用下均可增强HL-60细胞活性(P<0.05)。相比于sh-NC对照组,干扰linc00467的表达在0.1、0.2、0.3、0.4、0.5μg/mL阿霉素浓度作用下均可降低HL-60细胞活性(P<0.05)。与未处理组相比,阿霉素处理HL-60细胞后linc00467表达量升高(P<0.05)。结论linc00467有促进AML细胞对阿霉素耐药的生物学功能,为AML新的治疗药物开发提供了依据。
Objective To study the expression and function of long non-coding RNA linc00467 in childhood acute myeloid leukemia(AML).Methods Bone marrow samples were collected from 5 children with AML who were diagnosed from May 2016 to June 2018.Normal bone marrow samples based on bone marrow examination were collected from 3 children as controls.Quantitative real-time PCR was used to measure the expression of linc00467 in the two groups.A lentivirus system was used to achieve overexpression of linc00467 in AML cells(HL-60)(linc00467 overexpression group),and empty vector expressing green fluorescent protein(GFP)was transfected into AML cells to establish a GFP control group.A lentivirus system was used to insert an interfering sequence into AML cells(sh-linc00467 interfering group),and a random sequence was inserted to establish an sh-NC control group.Cell proliferation and resistance to doxorubicin were observed for all groups.Results Compared with the normal control group,the children with AML had a significant increase in linc00467(P=0.018).Overexpression and interference with linc00467 expression had no significant effect on cell proliferation.Compared with the GFP control group,the linc00467 overexpression group had a significant increase in the viability of HL-60 cells at the adriamycin concentrations of 0.1,0.2,0.3,0.4,and 0.5μg/mL(P<0.05).Compared with the sh-NC control group,the sh-linc00467 interfering group had a significant reduction in the viability of HL-60 cells at the adriamycin concentrations of 0.1,0.2,0.3,0.4,and 0.5μg/mL(P<0.05).Compared with the untreated group,the adriamycin treatment group had a significant increase in the expression of linc00467 in HL-60 cells(P<0.05).Conclusions This study reveals the biological function of linc00467 to promote the resistance to adriamycin in AML,which provides a basis for developing new therapeutic drugs for AML.
作者
饶春宝
雒东
林子添
谢明玉
胡媛
彭琪
江华
张振洪
陆小梅
RAO Chun-Bao;LUO Dong;LIN Zi-Tian;XIE Ming-Yu;HU Yuan;PENG Qi;JIANG Hua;ZHANG Zhen-Hong;LU Xiao-Mei(Key Laboratory of Genetics and Infectious Diseases,Dongguan Institute of Pediatrics,Dongguan,Guangdong 523327,China)
出处
《中国当代儿科杂志》
CAS
CSCD
北大核心
2020年第7期734-738,共5页
Chinese Journal of Contemporary Pediatrics
基金
广东省自然科学基金(2017A030310588)
东莞市社会科技发展重点项目(2017507150100445,20185071501001628)。
