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首页> 外文期刊>Cancer Management and Research >HIF1α/miR-520a-3p/AKT1/mTOR Feedback Promotes The Proliferation And Glycolysis Of Gastric Cancer Cells
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HIF1α/miR-520a-3p/AKT1/mTOR Feedback Promotes The Proliferation And Glycolysis Of Gastric Cancer Cells

机译：HIF1α/ miR-520A-3P / AKT1 / MTOR反馈促进胃癌细胞的增殖和糖溶解

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Purpose: Various microRNAs are involved in the development of gastric cancer (GC). This study investigated the role and mechanism of miR-520a-3p in GC. Method: Quantitative real-time fluorescence PCR (qRT-PCR) was applied to measure the expression level of miR-520a-3p in GC tissues and cell lines. The chi-squared test was employed to evaluate the relationship between the expression level of miR-520a-30p and clinical traits. The cell count kit-8 assay was used to detect the effect of miR-520a-3p on GC cell proliferation, while its effect on glycolysis was determined using the glucose assumption, lactate, and ATP production assay. The effect of miR-520a-3p on tumor growth in vivo was examined using a xenograft model. The relationship between miR-520a-30p and AKT1/mTOR/HIF1α pathway in normoxia and hypoxia was investigated using bioinformatics analysis, dual-luciferase reporter assay, qRT-PCR and Western blotting. Results: The expression of miR-520a-3p was decreased in GC tissues and cell lines. The expression level of miR-520a-3p was negatively associated with various malignant biological properties in patients. Overexpression/inhibition of miR-520a-3p decreased/promoted cell proliferation and glycolysis in vitro. Overexpression of miR-520a-3p inhibited tumor growth in vivo. AKT1 is the functional target of MiR-520a-3p, which was decreased in miR-520a-3p-overexpressing cells. In addition, overexpression of miR-520a-3p decreased the protein level of AKT1, mTOR, HIF1α, and target genes of HIF1α such as Glut1 and VEGF. Restoration of the expression of AKT1 can decrease the inhibitory effect of miR-520a-3p on the AKT1/mTOR/HIF1α pathway, as well as cell proliferation and glycolysis. Furthermore, the level of miR-520a-3p was decreased, while that of AKT1 was increased under hypoxia. Notably, inhibition of HIF1α or overexpression of miR-520a-3p suppressed these effects. Conclusion: Our study provided the first evidence for the existence of HIF1α/miR-520a-3p/AKT1/mTOR feedback, which promotes the proliferation and glycolysis of GC cells, highlighting a potential novel target for treatment.
机译：目的：各种MicroRNA参与胃癌（GC）的发展。本研究研究了MIR-520A-3P在GC中的作用和机制。方法：施用定量实时荧光PCR（QRT-PCR）测量GC组织和细胞系中miR-520a-3p的表达水平。使用Chi方检验来评估miR-520a-30p和临床特征的表达水平之间的关系。用于检测miR-520a-3p对GC细胞增殖对miR-520a-3p的影响，同时使用葡萄糖假设，乳酸和ATP生产测定法测定其对糖醇的影响。使用异种移植模型检查miR-520a-3p对体内肿瘤生长的影响。使用生物信息分析，双荧光素酶报告分析，QRT-PCR和Western印迹，研究了MiR-520A-30P和AKT​​1 / MTOR /HIF1α途径的关系。结果：GC组织和细胞系中miR-520a-3p的表达降低。 miR-520a-3p的表达水平与患者的各种恶性生物学性质负相关。过表达/抑制miR-520a-3p的促进/促进细胞增殖和体外糖酵解。 miR-520a-3p的过表达抑制体内肿瘤生长。 AKT1是miR-520a-3p的功能靶标，其在miR-520a-3p过表达细胞中降低。此外，miR-520a-3p的过表达降低了Hif1α的Akt1，mtor，Hif1α和靶基因，例如Glut1和VEGF。恢复AKT1的表达可以降低miR-520a-3p对Akt1 / mtor /hif1α途径的抑制作用，以及细胞增殖和糖醇。此外，MiR-520A-3P的水平降低，而AKT1的水平在缺氧下增加。值得注意的是，MIR-520A-3P的HIF1α或过表达的抑制抑制了这​​些效果。结论：我们的研究为存在HIF1α/ miR-520A-3P / AKT1 / MTOR反馈的第一种证据提供了GC细胞的增殖和糖溶解，突出了潜在的治疗靶标。

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