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首页> 外文期刊>Molecular medicine reports >MicroRNA-27a-3p promotes epithelial-mesenchymal transition by targeting NOVA alternative splicing regulator 1 in gastric cancer
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MicroRNA-27a-3p promotes epithelial-mesenchymal transition by targeting NOVA alternative splicing regulator 1 in gastric cancer

机译:MicroRNA-27A-3P通过靶向Nova替代剪接调节剂1在胃癌中促进上皮 - 间充质转换

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摘要

NOVA alternative splicing regulator 1 (NOVA1) dysregulation has been detected in the gastric cancer microenvironment. Decreased NOVA1 expression has been linked to the progression and poor prognosis of gastric cancer; however, the role of NOVA1 in regulating epithelial-mesenchymal transition (EMT) remains unclear in this disease. Experimental evidence has shown that miR-27a-3p is a potential oncogene in gastric cancer. In the present study, we observed that miR-27a-3p expression was increased in gastric cancer and was inversely associated with overall survival. Overexpression of miR-27a-3p promoted EMT in AGS gastric cancer cells. Additionally, overexpression of miR-27a-3p inhibited NOVA1 expression, while silencing of NOVA1 promoted EMT in AGS cells. A total of 108 gastric cancer samples were examined for NOVA1 expression by immunohistochemistry. Decreased NOVA1 expression was linked to lymph node metastasis, tumor-node-metastasis stage and shorter overall survival. Therefore, these results indicated that NOVA1 could be a potential tumor suppressive gene and that miR-27a-3p promotes EMT by targeting NOVA1 in gastric cancer.
机译:在胃癌微环境中检测到Nova替代剪接调节器1(Nova1)脱核。下降的Nova1表达已与胃癌的进展和差的预后有关;然而,Nova1在调节上皮 - 间充质转换(EMT)方面的作用仍不清楚这种疾病。实验证据表明MiR-27A-3P是胃癌中的潜在癌症。在本研究中,我们观察到MiR-27A-3P表达在胃癌中增加,与整体存活率相反。 miR-27a-3p的过度表达促进了AGS胃癌细胞的EMT。另外,miR-27a-3p的过表达抑制了Nova1表达,而Nova1的沉默在Ags细胞中促进了EMT。通过免疫组织化学检查Nova1表达的总共108个胃癌样品。 Nova1表达减少与淋巴结转移,肿瘤节点转移阶段和较短的整体存活率相关联。因此,这些结果表明Nova1可以是潜在的肿瘤抑制基因,并且MiR-27A-3P通过靶向Nova1在胃癌中促进EMT。

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