首页> 外文期刊>Experimental and therapeutic medicine >Overexpression of miR-574-3p suppresses proliferation and induces apoptosis of chronic myeloid leukemia cells via targeting IL6/JAK/STAT3 pathway
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Overexpression of miR-574-3p suppresses proliferation and induces apoptosis of chronic myeloid leukemia cells via targeting IL6/JAK/STAT3 pathway

机译:MiR-574-3P的过度表达抑制了通过靶向IL6 / JAK / Stat3途径抑制慢性髓性白血病细胞凋亡的增殖和诱导慢性骨髓白血病细胞凋亡

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摘要

The present study aimed to elucidate the potential roles and regulatory mechanism of microRNA (miR)-574-3p in the development of chronic myeloid leukemia (CML). The expression of miR-574-3p in peripheral blood obtained from patients with CML was examined. Subsequently, miR-574-3p was overexpressed and suppressed in CML K562 cells to further investigate the effects of miR-574-3p on cell proliferation, and apoptosis. Furthermore, a luciferase reporter assay was performed to investigate whether interleukin-6 (IL-6) was a target of miR-574-3p. In addition, the regulatory association between miR-574-3p and the IL-6/Janus kinase (JNK)/signal transducer and activator of transcription-3 (STAT3) signaling pathway was explored. The expression of miR-574-3p in the peripheral blood obtained from patients with CML was significantly lower compared with that in healthy controls. Overexpression of miR-574-3p significantly inhibited the proliferation and induced the apoptosis of K562 cells, whereas suppression of miR-574-3p exhibited opposite effects. In addition, IL-6 was identified to be a direct target of miR-574-3p. Overexpression of IL-6 significantly promoted the proliferation and inhibited the apoptosis of K562 cells. Furthermore, overexpression of miR-574-3p inhibited the activation of the JAK/STAT3 signaling pathway, which was rescued by overexpression of IL-6. The results of the current study indicate that miR-574-3p overexpression may serve an important role in inhibiting proliferation and inducing apoptosis of K562 cells via suppression of IL-6/JAK/STAT3 signaling pathway activation. miR-574-3p may serve as a potential therapeutic target for CML.
机译:本研究旨在阐明MicroRNA(MIR)-574-3P在慢性骨髓白血病(CML)的发育中的潜在作用和调节机制。检查了从CML患者获得的外周血中miR-574-3p的表达。随后,MIR-574-3P在CML K562细胞中过表达并抑制,进一步研究MIR-574-3P对细胞增殖和细胞凋亡的影响。此外,进行荧光素酶报告器测定以研究白细胞介素-6(IL-6)是miR-574-3p的靶标。此外,探讨了MiR-574-3P和IL-6 / Janus激酶(JNK)/信号传感器和转录-3(STAT3)信号传导途径的激活剂之间的调节关联。与健康对照组相比,CML患者的外周血中MIR-574-3P的表达显着降低。 miR-574-3p的过度表达显着抑制了增殖并诱导K562细胞的凋亡,而MiR-574-3P的抑制表现出相反的效果。此外,IL-6被鉴定为miR-574-3p的直接靶标。 IL-6的过度表达显着促进了增殖并抑制K562细胞的凋亡。此外,miR-574-3p的过表达抑制了jak / stat3信号传导途径的激活,该通路通过IL-6的过度表达来抵抗。目前研究的结果表明,MIR-574-3P过表达可用于抑制IL-6 / JAK / STAT3信号通路激活抑制K562细胞的增殖和诱导K562细胞凋亡的重要作用。 miR-574-3p可用作CML的潜在治疗靶标。

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