RETRACTED: miR-154 suppresses non-small cell lung cancer growth in vitro and in vivo (Retracted article. See vol. 49, 2023)

被引:31
|
作者
Lin, Xingyu [1 ]
Yang, Zhiguang [2 ]
Zhang, Peng [1 ]
Shao, Guoguang [1 ]
机构
[1] Jilin Univ, Dept Thorac Surg, Hosp 1, Changchun 130021, Jilin, Peoples R China
[2] Jilin Univ, Dept Anesthesiol, Hosp 1, Changchun 130021, Jilin, Peoples R China
关键词
microRNA; miR-154; non-small cell lung cancer; tumor growth; MESENCHYMAL TRANSITION; MICRORNAS; EMT; DYSREGULATION; METASTASIS; EXPRESSION; CLUSTER;
D O I
10.3892/or.2015.3895
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
miR-154 has been proven to act as a tumor suppressor in several types of tumors. However, its role in non-small cell lung cancer (NSCLC) remains unclear. Thus, the aim of this study was to investigate the effects of miR-154 on NSCLC tumorigenesis and development. Using real-time quantitative PCR (qRT-PCR), we analyzed expression of miR-154 at the transcriptional level in 40 NSCLC tumor tissues and matched adjacent normal tissues and the correlation with clinicopathological features of the patients. The miR-154 mimic was stably transfected into NSCLC A549 cells, and the effects of miR-154 on cancer cell proliferation, colony formation, cell cycle arrest, apoptosis, migration and invasion in vitro, and on the growth of in vivo xenografts were investigated. miR-154 expression levels were significantly downregulated in the NSCLC compared to the corresponding non-cancerous lung tissues (P<0.05), and decreased miR-154 expression was significantly associated with metastasis (P<0.001), larger tumor size (P<0.001) and advanced TNM stage (P<0.001). Furthermore, transfection of the miR-154 mimic into the NSCLC A549 cells was able to inhibit cell proliferation, colony formation, invasion and migration, and induce cell apoptosis and G0/G1 cell cycle arrest. Enforced expression of miR-154 also suppressed the growth of cancer cell xenografts in vivo. These findings indicate that miR-154 may become a potential target for miRbased therapy of NSCLC.
引用
收藏
页码:3053 / 3060
页数:8
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