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TEL-MN1 融合基因过表达增强 HL-60 细胞对伊达比星的耐药性。

Overexpression of TEL-MN1 Fusion Enhances Resistance of HL-60 Cells to Idarubicin.

机构信息

Department of Hematology, Institute of Hematology, Changhai Hospital, Second Military Medical University, Shanghai, China.

Department of Hematology, Institute of Hematology, Changhai Hospital, Second Military Medical University, Shanghai, China,

出版信息

Chemotherapy. 2018;63(6):308-314. doi: 10.1159/000495073. Epub 2019 Mar 6.

DOI:10.1159/000495073
PMID:30840968
Abstract

BACKGROUND

The translocation t(12; 22) (p13;q12) is a recurrent but infrequent chromosome abnormality in human myeloid malignancies. To date, the role of TEL-MN1 fusion in leukemogenic process and drug resistance is still largely unknown.

METHODS

In the present study, the TEL-MN1 fusion was transfected into HL-60 cells to upregulate TEL-MN1 expression via a retroviral vector. MTT assay was employed to examine cell viability and flow cytometry was performed to evaluate cell apoptosis. Idarubicin was used to treat HL-60 cells for estimating the effect of TEL-MN1 fusion on the chemotherapy resistance.

RESULTS

The results showed that overexpression of TEL-MN1 in HL-60 cells could promote cell proliferation, suggesting that TEL-MN1 may be involved in the leukemogenesis process. HL-60 cells treated with idarubicin showed a weakened cell viability, whereas TEL-MN1 overexpression attenuated the idarubicin-induced inhibition of cell viability and acceleration of cell apoptosis of HL-60 cells.

CONCLUSION

Taken together, our results indicated that TEL-MN1 fusion is an oncogene involved in the leukemogenesis process and TEL-MN1 overexpression enhanced resistance of HL-60 cells to idarubicin, which may provide a useful tool for studying the mechanism of leukemogenesis and drug resistance.

摘要

背景

t(12;22)(p13;q12)易位是人类髓系恶性肿瘤中一种常见但罕见的染色体异常。迄今为止,TEL-MN1 融合在白血病发生和耐药中的作用仍知之甚少。

方法

本研究通过逆转录病毒载体转染 HL-60 细胞,上调 TEL-MN1 表达,检测 TEL-MN1 融合对 HL-60 细胞活力和凋亡的影响。采用 MTT 法检测细胞活力,流式细胞术检测细胞凋亡,伊达比星(Idarubicin)处理 HL-60 细胞,评估 TEL-MN1 融合对化疗耐药的影响。

结果

结果表明,TEL-MN1 在 HL-60 细胞中的过表达可促进细胞增殖,提示 TEL-MN1 可能参与白血病的发生过程。伊达比星处理 HL-60 细胞后,细胞活力减弱,而过表达 TEL-MN1 可减弱伊达比星诱导的 HL-60 细胞活力抑制和细胞凋亡加速。

结论

综上所述,我们的研究结果表明,TEL-MN1 融合是一种参与白血病发生的癌基因,TEL-MN1 过表达增强了 HL-60 细胞对伊达比星的耐药性,为研究白血病发生和耐药的机制提供了有用的工具。

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