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α-2,3-唾液酸转移酶通过靶向ST3GAL1的miR-4701-5p调节慢性髓性白血病的多药耐药性。

Alpha-2, 3-sialyltransferases regulate the multidrug resistance of chronic myeloid leukemia through miR-4701-5p targeting ST3GAL1.

作者信息

Li Yan, Luo Shihua, Dong Weijie, Song Xiaobo, Zhou Huimin, Zhao Lifen, Jia Li

机构信息

College of Laboratory Medicine, Dalian Medical University, Dalian, Liaoning, China.

Department of Clinical Laboratory, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.

出版信息

Lab Invest. 2016 Jul;96(7):731-40. doi: 10.1038/labinvest.2016.50. Epub 2016 Apr 18.

Abstract

The aberrant sialylation profile on the surface of leukemia cells has been recognized for its potential diagnostic value towards assessing leukemia multidrug resistance (MDR). MicroRNAs as endogenous regulators of gene expression have been implicated in treating MDR. In this study, we describe the differential expressional profiles of α-2, 3-sialyltransferases (ST) and miR-4701-5p in three pairs of chronic myeloid leukemia (CML) cell lines and 48 clinical samples of bone marrow mononuclear cells from CML patients. The altered expression level of ST3GAL1 was found corresponding to the drug-resistant phenotype (with and without adriamycin resistance) of CML cell lines both in vitro and in vivo. Further the results showed that miR-4701-5p directly targeted ST3GAL1 to reduce CML cells resistance to multiple chemotherapeutics in vitro and to convert tumor cells from adriamycin resistant to susceptible in vivo of mice. These results indicate that differential expression of α-2,3 ST is involved in MDR of CML, and that miR-4701-5p regulates the susceptibility of CML cells to multiple drugs, at least in part, through targeting ST3GAL1.

摘要

白血病细胞表面异常的唾液酸化特征因其对评估白血病多药耐药性(MDR)的潜在诊断价值而受到认可。微小RNA作为基因表达的内源性调节因子,已被证明与治疗MDR有关。在本研究中,我们描述了三对慢性髓性白血病(CML)细胞系以及48例CML患者骨髓单个核细胞临床样本中α-2,3-唾液酸转移酶(ST)和miR-4701-5p的差异表达谱。发现在体外和体内,ST3GAL1表达水平的改变与CML细胞系的耐药表型(有无阿霉素耐药)相对应。此外,结果表明,miR-4701-5p直接靶向ST3GAL1,以降低CML细胞在体外对多种化疗药物的耐药性,并在小鼠体内将肿瘤细胞从阿霉素耐药转变为敏感。这些结果表明,α-2,3 ST的差异表达参与了CML的MDR,并且miR-4701-5p至少部分地通过靶向ST3GAL1来调节CML细胞对多种药物的敏感性。

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