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伊马替尼和波纳替尼对慢性髓性白血病自噬和微小RNA组的比较作用

Comparative effect of imatinib and ponatinib on autophagy and miRNome in chronic myeloid leukemia.

作者信息

Kayabasi Cagla, Okcanoglu Tugce Balci, Yelken Besra Ozmen, Asik Aycan, Susluer Sunde Yilmaz, Avci Cigir Biray, Saydam Guray, Gunduz Cumhur

机构信息

Department of Medical Biology, Faculty of Medicine, Ege University, Izmir 35100, Turkey.

Vocational School of Health Sciences, Near East University, Nicosia, TRNC, Cyprus.

出版信息

Gene. 2017 Dec 30;637:173-180. doi: 10.1016/j.gene.2017.09.036. Epub 2017 Sep 20.

Abstract

BCR-ABL tyrosine kinase inhibitors (TKIs) are selective therapies for the patients with Chronic Myeloid Leukemia (CML). Imatinib and ponatinib have remarkable long-term efficacy on a major molecular response. Although TKI related induction of cytotoxicity and apoptosis have been clearly investigated in molecular levels, their comparative effect on autophagy and miRNome are largely unknown. This study aimed to investigate the involvement of alterations of miRNA expressions in CML progression, and how imatinib and ponatinib affect this process, by comparing CML, imatinib-resistant CML and leukemia stem cells (LSC). Cytotoxicity analysis was conducted by WST-1, apoptosis was evaluated by AnnexinV, autophagy was analyzed by Tb/GFP TR-FRET LC3B assay and changes in miRNomes were evaluated with microarray method. Ponatinib showed higher cytotoxicity and apoptosis at far fewer concentrations than imatinib. Both imatinib and ponatinib was able to trigger autophagy in imatinib-resistant K562ima3 cell line but not in LSC. We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766. This study is the first comparative miRNome analysis of CML, resistant CML and LSCs following the imatinib or ponatinib treatment and may guide to identify new markers for diagnosis, follow-up of the disease and to develop novel therapeutic strategies if supported by preclinical studies.

摘要

BCR-ABL酪氨酸激酶抑制剂(TKIs)是慢性髓性白血病(CML)患者的选择性治疗药物。伊马替尼和波纳替尼对主要分子反应具有显著的长期疗效。尽管在分子水平上已经对TKI相关的细胞毒性和凋亡诱导进行了明确研究,但它们对自噬和微小RNA组的比较作用在很大程度上尚不清楚。本研究旨在通过比较CML、伊马替尼耐药的CML和白血病干细胞(LSC),研究微小RNA表达改变在CML进展中的作用,以及伊马替尼和波纳替尼如何影响这一过程。通过WST-1进行细胞毒性分析,通过膜联蛋白V评估凋亡,通过Tb/GFP TR-FRET LC3B检测分析自噬,并采用微阵列方法评估微小RNA组的变化。与伊马替尼相比,波纳替尼在低得多的浓度下就表现出更高的细胞毒性和凋亡率。伊马替尼和波纳替尼都能够在伊马替尼耐药的K562ima3细胞系中触发自噬,但在LSC中则不能。我们指出,伊马替尼和波纳替尼会引起显著的微小RNA谱改变,特别是在miR-214-pre、miR-218、miR-19a-5p、miR-19b-1-5p、miR-27b-pre、miR-23b-pre、miR-320e、miR-200a-pre、miR-508-3p、miR-33-pre和miR-766的表达方面。本研究是首次对伊马替尼或波纳替尼治疗后的CML、耐药CML和LSCs进行的比较微小RNA组分析,如果得到临床前研究的支持,可能有助于识别新的诊断标志物、疾病随访标志物,并制定新的治疗策略。

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