Long non-coding RNA HOXA11-AS inhibits apoptosis, induces proliferation, and promotes autophagy via the miR-214-3p/ATG12 axis in acute T lymphoblastic leukemia

IF 2.2 4区 生物学 Q3 CELL BIOLOGY
Rui Zhang, YuanYuan Zhang, XiaoFei Li, ShaoHua Wang, Jiao Li, ShuoChun Shao, Bin Liu, WeiWei Guo, Min Shi
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引用次数: 0

Abstract

Acute T lymphocytic leukemia (T-ALL) is a hematological cancer with high mortality. The literature suggests an association between T-ALL and Long non-coding RNAs (lncRNAs). Nevertheless, the mechanism of lncRNA HOXA11-AS in T-ALL remains undetermined. The lncRNA HOXA11-AS expression level were assessed in T-ALL patients and normal controls by qRT-PCR. Furthermore, The proliferation, apoptosis, and autophagy of T-ALL cell (Molt4 and Jurkat cells) were investigated in vitro via EdU incorporation experiment, flow cytometry, immunofluorescence, and Western blotting. Moreover, the relationship between HOXA11-AS and miR-214-3p and between miR-214-3p, and ATG12 was verified via dual-luciferase reporter assays. Our investigation demonstrated that compared to normal controls, the HOXA11-AS expression level were increased in T-ALL patients. Furthermore, in T-ALL cells, inhibition of HOXA11-AS or overexpression of miR-214-3p reduced autophagy and proliferation, while stimulating apoptosis. However, miR-214-3p inhibition counteracted HOXA11-AS-mediated suppression of T-ALL cell proliferation, autophagy, and apoptosis. In addition, HOXA11-AS modulated ATG12 via sponging miR-214-3p. Overall, this research indicated that lncRNA HOXA11-AS not only stimulates cell proliferation and autophagy but also inhibits apoptosis via the miR-214-3p/ATG12 axis, thereby suggesting that lncRNA HOXA11-AS might be a new candidate for T-ALL diagnosis and therapy.

在急性T淋巴细胞白血病中,长链非编码RNA HOXA11-AS通过miR-214-3p/ATG12轴抑制细胞凋亡,诱导细胞增殖,促进细胞自噬
急性T淋巴细胞白血病(T- all)是一种高死亡率的血液学癌症。文献表明T-ALL与长链非编码rna (lncRNAs)之间存在关联。然而,lncRNA HOXA11-AS在T-ALL中的作用机制尚未确定。采用qRT-PCR检测T-ALL患者和正常对照中lncRNA HOXA11-AS的表达水平。此外,通过EdU掺入实验、流式细胞术、免疫荧光和Western blotting检测T-ALL细胞(Molt4和Jurkat细胞)的增殖、凋亡和自噬。此外,HOXA11-AS与miR-214-3p之间以及miR-214-3p与ATG12之间的关系通过双荧光素酶报告基因检测得到验证。我们的研究表明,与正常对照相比,T-ALL患者的HOXA11-AS表达水平升高。此外,在T-ALL细胞中,抑制HOXA11-AS或过表达miR-214-3p可减少自噬和增殖,同时刺激细胞凋亡。然而,miR-214-3p抑制抵消了hoxa11 - as介导的T-ALL细胞增殖、自噬和凋亡的抑制。此外,HOXA11-AS通过海绵miR-214-3p调节ATG12。综上所述,本研究表明,lncRNA HOXA11-AS不仅可以刺激细胞增殖和自噬,还可以通过miR-214-3p/ATG12轴抑制细胞凋亡,从而提示lncRNA HOXA11-AS可能是T-ALL诊断和治疗的新候选分子。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Molecular Histology
Journal of Molecular Histology 生物-细胞生物学
CiteScore
5.90
自引率
0.00%
发文量
68
审稿时长
1 months
期刊介绍: The Journal of Molecular Histology publishes results of original research on the localization and expression of molecules in animal cells, tissues and organs. Coverage includes studies describing novel cellular or ultrastructural distributions of molecules which provide insight into biochemical or physiological function, development, histologic structure and disease processes. Major research themes of particular interest include: - Cell-Cell and Cell-Matrix Interactions; - Connective Tissues; - Development and Disease; - Neuroscience. Please note that the Journal of Molecular Histology does not consider manuscripts dealing with the application of immunological or other probes on non-standard laboratory animal models unless the results are clearly of significant and general biological importance. The Journal of Molecular Histology publishes full-length original research papers, review articles, short communications and letters to the editors. All manuscripts are typically reviewed by two independent referees. The Journal of Molecular Histology is a continuation of The Histochemical Journal.
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