[长链非编码RNA linc00467在儿童急性髓系白血病中的表达及其在耐药中的作用]
[Expression of long non-coding RNA linc00467 in childhood acute myeloid leukemia and its role in drug resistance].
作者信息
Rao Chun-Bao, Luo Dong, Lin Zi-Tian, Xie Ming-Yu, Hu Yuan, Peng Qi, Jiang Hua, Zhang Zhen-Hong, Lu Xiao-Mei
机构信息
Key Laboratory of Genetics and Infectious Diseases, Dongguan Institute of Pediatrics, Dongguan, Guangdong 523327, China.
出版信息
Zhongguo Dang Dai Er Ke Za Zhi. 2020 Jul;22(7):734-738. doi: 10.7499/j.issn.1008-8830.2002007.
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 0.5 μg/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 0.5 μg/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.
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
收集2016年5月至2018年6月确诊的5例儿童AML患者的骨髓样本。选取3例经骨髓检查为正常的儿童骨髓样本作为对照。采用定量实时PCR检测两组中linc00467的表达。利用慢病毒系统使AML细胞（HL-60）中linc00467过表达（linc00467过表达组），并将表达绿色荧光蛋白（GFP）的空载体转染至AML细胞中建立GFP对照组。利用慢病毒系统将干扰序列导入AML细胞（sh-linc00467干扰组），并导入随机序列建立sh-NC对照组。观察所有组的细胞增殖及对阿霉素的耐药性。
结果
与正常对照组相比，AML患儿linc00467显著升高（P = 0.018）。linc00467过表达及干扰其表达对细胞增殖无显著影响。与GFP对照组相比，在阿霉素浓度为0.1、0.2、0.3、0.4和0.5 μg/mL时，linc00467过表达组HL-60细胞活力显著升高（P < 0.05）。与sh-NC对照组相比，在阿霉素浓度为0.1、0.2、0.3、0.4和0.5 μg/mL时，sh-linc00467干扰组HL-60细胞活力显著降低（P < 0.05）。与未处理组相比，阿霉素处理组HL-60细胞中linc00467表达显著升高（P < 0.05）。
结论
本研究揭示了linc00467促进AML对阿霉素耐药的生物学功能，为开发AML新型治疗药物提供了依据。
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