Chang Yongmei, Yan Wensen, Sun Cong, Liu Qingfeng, Wang Jun, Wang Mingzhi
Department of Respiratory Medicine, Guangdong No. 2 Provincial People Hospital, Guangzhou, Guangdong 510317, P.R. China.
Department of Cardiothoracic Surgery, Guangdong No. 2 Provincial People Hospital, Guangzhou, Guangdong 510317, P.R. China.
Oncol Lett. 2017 Dec;14(6):6923-6928. doi: 10.3892/ol.2017.7092. Epub 2017 Sep 28.
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.
肺癌是最常见的肿瘤类型之一,也是全球癌症相关死亡的主要原因。此外,非小细胞肺癌(NSCLC)占所有肺癌病例的约80%。上皮-间质转化(EMT)是一个重要的细胞生物学过程,与癌症的迁移、转移、哮喘和肺部纤维化有关。在本研究中,发现miR-145-5p能够通过使NSCLC细胞中的c-Jun氨基末端激酶(JNK)信号通路失活来抑制EMT。丝裂原活化蛋白激酶激酶激酶1(MAP3K1)被预测并证实为miR-145-5p的一个新靶点。MAP3K1的过表达能够通过JNK信号通路逆转miR-145-5p对EMT的抑制作用。总体而言,结果表明miR-145-5p在NSCLC细胞中通过靶向MAP3K1经由JNK信号通路抑制EMT。