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首页> 外文期刊>European review for medical and pharmacological sciences. >DUXAP10 regulates proliferation and apoptosis of chronic myeloid leukemia via PTEN pathway
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DUXAP10 regulates proliferation and apoptosis of chronic myeloid leukemia via PTEN pathway

机译:DUXAP10通过PTEN途径调节慢性粒细胞白血病的增殖和凋亡

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摘要

OBJECTIVE: To investigate the role of DUXAP10 in chronic myelogenous leukemia (CML) and its underlying mechanism. PATIENTS AND METHODS: We detected DUXAP10 expression in 82 CML patients, 12 normal controls, and CML cell line by qRT-PCR (quantitative real-time polymerase chain reaction). After transfection of si-DUXAP10 or si-PTEN in CML cell lines (K652, KG-1), we detected proliferation, cell cycle, and apoptosis by CCK-8 (cell counting kit-8), colony formation assay, and flow cytometry, respectively. Finally, protein expressions of p21, CDK2, Bcl-2, Bax, and PTEN were detected by Western blot. RESULTS: DUXAP10 was upregulated in CML tissues and cells, which was gradually increased in the chronic phase (CP), acceleration phase (AP), and blast phase (BP) of CML. Knockdown of DUXAP10 in K652 and KG-1 cells can remarkably inhibit cell proliferation, promote cycle arrest and apoptosis. Western blot and flow cytometry results demonstrated that DUXAP10 can reduce apoptosis by inhibiting PTEN expression. CONCLUSIONS: Overexpressed DUXAP10 accelerates the development and progression of CML by promoting cell proliferation, reducing cell cycle arrest and apoptosis via inhibiting PTEN expression.
机译:目的:探讨DUXAP10在慢性粒细胞白血病(CML)中的作用及其潜在机制。患者和方法:我们通过qRT-PCR(定量实时聚合酶链反应)检测了82名CML患者,12名正常对照和CML细胞系中DUXAP10的表达。在CML细胞系(K652,KG-1)中转染si-DUXAP10或si-PTEN后,我们通过CCK-8(细胞计数试剂盒8),集落形成分析和流式细胞仪检测了增殖,细胞周期和凋亡, 分别。最后,通过Western印迹检测p21,CDK2,Bcl-2,Bax和PTEN的蛋白表达。结果:DUXAP10在CML组织和细胞中上调,在CML的慢性期(CP),加速期(AP)和爆炸期(BP)逐渐升高。敲除DUXAP10在K652和KG-1细胞中可以显着抑制细胞增殖,促进周期停滞和凋亡。蛋白质印迹和流式细胞仪结果表明,DUXAP10可以通过抑制PTEN表达来减少细胞凋亡。结论:过表达的DUXAP10通过促进细胞增殖,通过抑制PTEN表达减少细胞周期停滞和凋亡而加速了CML的发展和进程。

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