In recent years, increasing number of lncRNAs have been studied in lung adenocarcinoma (LAD). LncRNA HOXA10-AS was found to be upregulated in LAD tissues. Based on the data of TCGA database, HOXA10-AS was a prognostic factor for lung adenocarcinoma. This study aims to reveal the biological function of HOXA10-AS in LAD. qRT-PCR was applied to test expression levels of HOXA10-AS in both LAD tissues and cell lines. Next, transcription factor ELK1 was demonstrated to upregulate HOXA10-AS in LAD cells through performing bioinformatics analysis and dual luciferase activity. Loss of function assays were performed in two different LAD cell lines. Silenced HOXA10-AS was proved to inhibit LAD progression by affecting cell proliferation, cell apoptosis and cell metastasis and EMT progress. Western blot analysis revealed that HOXA10-AS increased Wnt/beta-catenin signaling in LAD cell lines. Finally, rescue assays were carried out to identify the biological function of HOXA10-AS-Wnt/beta-catenin signaling in LAD progression. In conclusion, ELK1-induced upregulation of HOXA10-AS improved LAD progression through increasing Wnt/beta catenin signaling. (C) 2018 Published by Elsevier Inc.
第一作者机构:[1]Shanghai Jiao Tong Univ, Tongren Hosp, Dept Gerontol, Sch Med, 1111 Xianxia St, Shanghai 200336, Peoples R China
通讯作者:
推荐引用方式(GB/T 7714):
Sheng Kai,Lu Jiahuan,Zhao Hui.ELK1-induced upregulation of lncRNA HOXA10-AS promotes lung adenocarcinoma progression by increasing Wnt/beta-catenin signaling[J].BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS.2018,501(3):612-618.doi:10.1016/j.bbrc.2018.04.224.
APA:
Sheng, Kai,Lu, Jiahuan&Zhao, Hui.(2018).ELK1-induced upregulation of lncRNA HOXA10-AS promotes lung adenocarcinoma progression by increasing Wnt/beta-catenin signaling.BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,501,(3)
MLA:
Sheng, Kai,et al."ELK1-induced upregulation of lncRNA HOXA10-AS promotes lung adenocarcinoma progression by increasing Wnt/beta-catenin signaling".BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 501..3(2018):612-618