期刊
MOLECULAR THERAPY-NUCLEIC ACIDS
卷 22, 期 -, 页码 981-993出版社
CELL PRESS
DOI: 10.1016/j.omtn.2020.09.020
关键词
-
Lung adenocarcinoma (LUAD) is a predominant type of lung cancer in never-smoker patients. In this study, we identified a long noncoding RNA (lncRNA) LINC00857 that might regulate radio-sensitivity of LUAD cells. Expression of LINC00857 and baculoviral IAP repeat containing 5 (BIRC5) was determined to be upregulated in LUAD cells and tissues using qRT-PCR and western blot analysis. The correlation between LINC00857 and nuclear factor kappa B subunit 1 (NF-kappa B1) was verified using RNA immunoprecipitation and chromatin immunoprecipitation assays, while the binding relationship between NF-kappa B1 and BIRC5 was determined by dualluciferase reporter assay. It was suggested that LINC00857 could recruit NF-kappa B1 in BIRC5 promoter region. BIRC5 promoter activity was repressed in response to small interferingLINC00857 (si-LINC00857) in LUAD cells. Silencing LINC00857 or BIRC5 reduced proliferation and colony formation but enhanced apoptosis and radio-sensitivity of LUAD cells. The experiment in vivo verified the function of silencing LINC00857 on enhancing radio-sensitivity of LUAD cells. Our results reveal a functional regulatory LINC00857-NF-kappa B1-BIRC5 triplet in LUAD cells, suggesting LINC00857 as a potential target for LUAD treatment.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据