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首页> 外文期刊>Oncology letters >miR-145-5p inhibits epithelial-mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non-small cell lung cancer cells
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miR-145-5p inhibits epithelial-mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non-small cell lung cancer cells

机译:MiR-145-5P通过在非小细胞肺癌细胞中靶向MAP3K1来抑制通过JNK信号传导途径的上皮 - 间充质转换

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摘要

Lung cancer is one of the most common types of tumors and the leading cause of cancer-associated mortality in the world. Additionally, non-small cell lung cancer (NSCLC) accounts for similar to 80% of all lung cancer cases. Epithelial-mesenchymal transition (EMT) is an important cell biological process, which is associated with cancer migration, metastasis, asthma and fibrosis in the lung. In the present study, it was revealed that miR-145-5p was able to suppress EMT by inactivating the c-Jun N-terminal kinase (JNK) signaling pathway in NSCLC cells. Mitogen-activated protein kinase kinase kinase 1 (MAP3K1) was predicted and confirmed to be a novel target of miR-145-5p. Overexpression of MAP3K1 was able to reverse the inhibition of EMT induced by miR-145-5p via the JNK signaling pathway. Overall, the results revealed that miR-145-5p inhibits EMT via the JNK signaling pathway by targeting MAP3K1 in NSCLC cells.
机译:肺癌是世界上最常见的肿瘤类型之一,是世界上癌症相关死亡的主要原因之一。 此外,非小细胞肺癌(NSCLC)占所有肺癌病例的80%。 上皮 - 间充质转换(EMT)是一种重要的细胞生物过程,与肺中的癌症迁移,转移,哮喘和纤维化有关。 在本研究中,揭示了MIR-145-5P能够通过在NSCLC细胞中灭活C-JUN N-末端激酶(JNK)信号传导途径来抑制EMT。 预测丝裂原激活的蛋白激酶激酶激酶1(MAP3K1)并确认是miR-145-5p的新靶标。 MAP3K1的过表达能够通过JNK信号通路逆转MIR-145-5P诱导的EMT的抑制。 总的来说,结果显示MiR-145-5P通过在NSCLC细胞中靶向MAP3K1,通过JNK信号通路抑制EMT。

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