波形蛋白
癌症研究
上皮-间质转换
转染
肺癌
细胞生长
非小细胞肺癌
实时聚合酶链反应
免疫印迹
生物
免疫组织化学
下调和上调
基因
医学
肿瘤科
A549电池
免疫学
生物化学
遗传学
作者
Gao Yp,Li Y,Li Hj,B.-M. Zhao
标识
DOI:10.26355/eurrev_201909_19011
摘要
Objective The aim of this study was to identify the role of long non-coding RNA (lncRNA) NBR2 in non-small-cell lung cancer (NSCLC) and its possible molecular mechanisms. Patients and methods The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to explore lncRNA NBR2 expression in NSCLC cells and tissues. The chi-square test was used to analyze the relationship between lncRNA NBR2 expression and the clinical features of NSCLC patients. The pcDNA3.1 and pcDNA3.1-NBR2 vectors were transfected into NSCLC cells, and the proliferation and migration ability of NSCLC cells were detected using cell counting kit-8 (CCK-8) and transwell assay. The epithelial-mesenchymal transition (EMT)-related genes expression was detected by an EMT RT2 PCR array. QRT-PCR and Western blot was used to analyze the mRNA and protein levels of Notch1, Vimentin, N-cadherin, E-cadherin, HEY1, HEY2, and HEYL. Results The expression of lncRNA NBR2 was decreased in NSCLC patients tissues, and the NSCLC patients in the NBR2 low expression group showed a poor prognosis. Meanwhile, the expression of NBR2 in patients with NSCLC was correlated with tumor size. Overexpression of NBR2 suppressed the viability and migration of NSCLC cells and the expression of Notch1 and EMT-related genes in AsPC-1 cells. Simultaneous overexpression of NBR2 and Notch1 could reverse the inhibitory effect of NBR2 on proliferation and migration of NSCLC cells. Conclusions LncRNA NBR2 inhibited the progression of EMT in NSCLC by regulating the Notch1 pathway.
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