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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通过靶向非小细胞肺癌细胞中的MAP3K1通过JNK信号通路抑制上皮-间质转化

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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 ~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:肺癌是最常见的肿瘤类型之一,也是世界上与癌症相关的死亡率的主要原因。此外,非小细胞肺癌(NSCLC)约占所有肺癌病例的80%。上皮-间质转化(EMT)是重要的细胞生物学过程,与癌症的迁移,转移,哮喘和肺纤维化有关。在本研究中,揭示了miR-145-5p能够通过灭活NSCLC细胞中的c-Jun N端激酶(JNK)信号通路来抑制EMT。预测并证实丝裂原活化的蛋白激酶激酶激酶1(MAP3K1)是miR-145-5p的新型靶标。 MAP3K1的过表达能够通过JNK信号通路逆转miR-145-5p诱导的EMT抑制。总体而言,结果表明,miR-145-5p通过靶向NSCLC细胞中的MAP3K1,通过JNK信号通路抑制EMT。

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