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首页> 外文期刊>Journal of biochemical and molecular toxicology >Circular RNA circHIAT1 inhibits proliferation and epithelial-mesenchymal transition of gastric cancer cell lines through downregulation of miR-21
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Circular RNA circHIAT1 inhibits proliferation and epithelial-mesenchymal transition of gastric cancer cell lines through downregulation of miR-21

机译：圆形RNA Circhiat1通过MiR-21的下调抑制胃癌细胞系的增殖和上皮间过渡

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摘要

Gastric cancer (GC) is the third leading cause of cancer-related death worldwide. Circular RNA circHIAT1 has been proved to play an antitumor role. We aimed to explore the function and mechanism of circHIAT1 in GC. MKN28 and MKN45 cells were transfected with PLCDH-circHIAT1, miR-21 mimic, and relative control. Cell viability and apoptosis were examined through Cell Counting Kit-8 and flow cytometry, respectively. CircHIAT1 expression and other relative factors were tested through quantitative reverse transcription-polymerase chain reaction and Western blot analysis, respectively. Our findings demonstrated that circHIAT1 was lowly expressed in GC tissues. After transfection with PLCDH-circHIAT1 in MKN28 and MKN45 cells, cell viability was decreased, while the expression levels of p53 and p21 were raised, as well as apoptosis. Besides this, the epithelial-mesenchymal transition process was inhibited by PLCDH-circHIAT1 transfection. Mechanistically, miR-21 expression was upregulated in GC tissues and could be negatively regulated by circHIAT1. Further experiments showed that the addition of miR-21 mimic reversed the growth inhibition effects of circHIAT1 overexpression. Moreover, circHIAT1 inhibited the activation of phosphatase and tensin homolog/phosphatidylinositol 3 kinase/protein kinase B and extracellular signal-regulated kinase signal pathways via downregulating miR-21. CircHIAT1 functioned as a tumor inhibitor in GC cells through downregulating miR-21, and could be a novel target for GC treatment.
机译：胃癌（GC）是全球第三大癌症相关死亡原因。环状RNA circHIAT1已被证明具有抗肿瘤作用。我们旨在探讨circHIAT1在GC中的作用和机制。用PLCDH-circHIAT1、miR-21模拟物和相对对照转染MKN28和MKN45细胞。分别通过细胞计数试剂盒8和流式细胞仪检测细胞活力和凋亡。分别通过定量逆转录聚合酶链反应和Western blot分析检测CircHIAT1表达和其他相关因子。我们的研究结果表明circHIAT1在GC组织中低表达。在MKN28和MKN45细胞中转染PLCDH-circHIAT1后，细胞活力降低，而p53和p21的表达水平升高，以及细胞凋亡。此外，PLCDH-circHIAT1转染抑制了上皮-间质转化过程。从机制上讲，miR-21在GC组织中的表达上调，并可能受到circHIAT1的负调控。进一步的实验表明，添加miR-21模拟物逆转了circHIAT1过度表达的生长抑制效应。此外，circHIAT1通过下调miR-21抑制磷酸酶和张力蛋白同系物/磷脂酰肌醇3激酶/蛋白激酶B以及细胞外信号调节激酶信号通路的激活。CircHIAT1通过下调miR-21在GC细胞中发挥肿瘤抑制剂的作用，可能成为GC治疗的新靶点。

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