当前位置: X-MOL 学术Hum. Cell › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
miR-362-5p promotes cell proliferation and cell cycle progression by targeting GAS7 in acute myeloid leukemia.
Human Cell ( IF 4.3 ) Pub Date : 2020-01-10 , DOI: 10.1007/s13577-019-00319-4
Fuqun Wu 1, 2 , Changxin Yin 3 , Junhua Qi 1 , Deyu Duan 1 , Xi Jiang 1 , Jianhua Yu 2 , Zhaofan Luo 2
Affiliation  

Recently, miR-362-5p has attracted special interest as a novel prognostic predictor in acute myeloid leukemia (AML). However, its biological function and underlying molecular mechanism in AML remain to be further defined. Herein, we found that a significant increase in miR-362-5p expression was observed in AML patients and cell lines using quantitative real-time PCR. The expression of miR-362-5p was altered in THP-1 and HL-60 cells by transfecting with miR-362-5p mimic or inhibitor. A series of experiments showed that inhibition of miR-362-5p expression significantly suppressed cell proliferation, induced G0/G1 phase arrest and attenuated tumor growth in vivo. On the contrary, ectopic expression of miR-362-5p resulted in enhanced cell proliferation, cell cycle progression and tumor growth. Moreover, growth arrest-specific 7 (GAS7) was confirmed as a direct target gene of miR-362-5p and was negatively modulated by miR-362-5p. GAS7 overexpression imitated the tumor suppressive effect of silenced miR-362-5p on THP-1 cells. Furthermore, miR-362-5p knockdown or GAS7 overexpression obviously down-regulated the expression levels of PCNA, CDK4 and cyclin D1, but up-regulated p21 expression. Collectively, our findings demonstrate that miR-362-5p exerts oncogenic effects in AML by directly targeting GAS7, which might provide a promising therapeutic target for AML.

中文翻译:

miR-362-5p 通过靶向 GAS7 在急性髓性白血病中促进细胞增殖和细胞周期进程。

最近,miR-362-5p 作为急性髓性白血病 (AML) 的新型预后预测因子引起了人们的特别关注。然而,其在 AML 中的生物学功能和潜在的分子机制仍有待进一步确定。在此,我们发现使用定量实时 PCR 在 AML 患者和细胞系中观察到 miR-362-5p 表达显着增加。通过转染 miR-362-5p 模拟物或抑制剂,可以改变 THP-1 和 HL-60 细胞中 miR-362-5p 的表达。一系列实验表明,抑制 miR-362-5p 表达可显着抑制细胞增殖,诱导 G0/G1 期阻滞并减弱体内肿瘤生长。相反,miR-362-5p的异位表达导致细胞增殖、细胞周期进展和肿瘤生长增强。而且,生长停滞特异性 7 (GAS7) 被证实是 miR-362-5p 的直接靶基因,并受到 miR-362-5p 的负调控。GAS7 过表达模仿沉默的 miR-362-5p 对 THP-1 细胞的肿瘤抑制作用。此外,miR-362-5p敲低或GAS7过表达明显下调PCNA、CDK4和cyclin D1的表达水平,但上调p21的表达。总的来说,我们的研究结果表明,miR-362-5p 通过直接靶向 GAS7 在 AML 中发挥致癌作用,这可能为 AML 提供有希望的治疗靶点。CDK4 和 cyclin D1,但 p21 表达上调。总的来说,我们的研究结果表明,miR-362-5p 通过直接靶向 GAS7 在 AML 中发挥致癌作用,这可能为 AML 提供有希望的治疗靶点。CDK4 和 cyclin D1,但 p21 表达上调。总的来说,我们的研究结果表明,miR-362-5p 通过直接靶向 GAS7 在 AML 中发挥致癌作用,这可能为 AML 提供有希望的治疗靶点。
更新日期:2020-01-10
down
wechat
bug