Silencing LINC00511 inhibits cell proliferation, migration, and epithelial–mesenchymal transition via the PTEN–AKT–FOXO1 signaling pathway in lung cancer

被引:10
作者
Jiang L. [1 ]
Xie X. [1 ]
Ding F. [1 ]
Mei J. [1 ]
Bi R. [1 ]
机构
[1] Department of Cardiothoracic Surgery, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai
基金
中国国家自然科学基金;
关键词
EMT; FOXO1; LINC00511; lung cancer; migration; PTEN;
D O I
10.1139/bcb-2018-0364
中图分类号
学科分类号
摘要
Lung cancer is the most common cause of cancer-related death worldwide. Long noncoding RNAs (lncRNAs) are longer than 200 nt transcripts and are not translated into proteins. Increasing evidence has shown that lncRNAs are associated with several biological processes in cancer. However, the roles of LINC00511 in lung cancer progression remain unknown. In the present study, we confirmed that LINC00511 knockdown significantly inhibited cell proliferation and migration in A549, SPCA1, and H460 cells. Western blot results showed that silencing LINC00511 inhibited epithelial– mesenchymal transition (EMT), which resulted in decreased expression levels of ZEB2, N-cadherin, and vimentin and increased expression levels of E-cadherin. Additionally, silencing LINC00511 significantly upregulated PTEN mRNA and protein expression, increased FOXO1, and inactivated AKT. Furthermore, we found that PTEN knockdown reversed the inhibition of cell migration and proliferation induced by LINC00511 siRNA, markedly reduced p-FOXO1 expression, and promoted p-AKT expression and EMT in A549 and H460 cells. Therefore, these findings revealed that LINC00511 functions as an oncogene through the PTEN–AKT–FOXO1 signaling pathway in lung cancer, providing a potential target of metastasis in lung cancer. © 2021, Canadian Science Publishing. All rights reserved.
引用
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页码:1 / 8
页数:7
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