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首页> 外文期刊>Biochimica et biophysica acta. Molecular cell research >Epigenetic regulation of microRNA-128a expression contributes to the apoptosis-resistance of human T-cell leukaemia Jurkat cells by modulating expression of Fas-associated protein with death domain (FADD)
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Epigenetic regulation of microRNA-128a expression contributes to the apoptosis-resistance of human T-cell leukaemia Jurkat cells by modulating expression of Fas-associated protein with death domain (FADD)

机译：microRNA-128a表达的表观遗传调控通过调节具有死亡结构域（FADD）的Fas相关蛋白的表达来促进人T细胞白血病Jurkat细胞的凋亡抗性

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摘要

Increased expression of miR-128a is often observed in acute lymphoblastic leukaemia (ALL) compared with its expression in acute myeloid leukaemia (AML). The objective of this study was to investigate the role of miR-128a, especially that in the Fas-signalling pathway, in T-cell leukaemia cells. The role of miR-128a in Fas-mediated apoptosis was examined by using Fas-activating antibody (CH-11)-susceptible Jurkat cells and -resistant Jurkat/R cells. Whereas ectopic expression of miR-128a conferred Fas-resistance on Jurkat cells by directly targeting Fas-associated protein with death domain (FADD), antagonizing miR-128a expression sensitized Jurkat/R cells to the Fas-mediated apoptosis through derepression of FADD expression. Myeloid leukaemia HL60 and K562 cells were also CH-11-resistant, sharing a similar resistant mechanism with Jurkat/R cells. Furthermore, CH-11 induced demethylation of the promoter region of miR-128a with resultant up-regulation of miR-128a expression in Jurkat/R cells, which was shown to be a mechanism for the resistance of Jurkat/R cells to Fas-mediated apoptosis. Our results indicate that the induction of miR-128a expression by DNA demethylation is a novel mechanism of resistance to Fas-mediated apoptosis.
机译：与在急性髓细胞性白血病（AML）中的表达相比，在急性淋巴细胞性白血病（ALL）中经常观察到miR-128a的表达增加。这项研究的目的是研究miR-128a在T细胞白血病细胞中的作用，尤其是在Fas信号通路中的作用。通过使用Fas激活抗体（CH-11）敏感的Jurkat细胞和耐药的Jurkat / R细胞，检查了miR-128a在Fas介导的细胞凋亡中的作用。 miR-128a的异位表达通过直接靶向具有死亡域（FADD）的Fas相关蛋白而赋予Jurkat细胞Fas耐药性，而miR-128a表达的拮抗作用则是通过抑制FADD表达抑制Jurkat / R细胞对Fas介导的细胞凋亡的敏感性。髓样白血病HL60和K562细胞也具有CH-11-耐药性，与Jurkat / R细胞具有相似的耐药机制。此外，CH-11诱导了miR-128a启动子区域的去甲基化，并导致Jurkat / R细胞中miR-128a表达的上调，这被证明是Jurkat / R细胞对Fas介导的抗性的机制。细胞凋亡。我们的结果表明，通过DNA脱甲基作用诱导miR-128a表达是抵抗Fas介导的细胞凋亡的新机制。

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