期刊
AGING-US
卷 11, 期 9, 页码 2812-2821出版社
IMPACT JOURNALS LLC
DOI: 10.18632/aging.101953
关键词
LINC00857; esophageal adenocarcinoma; proliferation; apoptosis
资金
- National Natural Science Foundation of China (NSFC) [81702270, 81871883, 81803564]
- Affiliated Hospital of Guangdong Medical University Doctoral Foundation [2018052638]
- Guangxi Natural Science Foundation [2015GXNSF BA139117]
- China Postdoctoral Science Foundation [2018M633619XB]
- Medical Discipline Reserve Talents of Yunnan Province [H-2017037]
Esophageal adenocarcinoma (EAC) is one of the leading causes of cancer-related death worldwide, and the molecular biology of this cancer remains poorly understood. Recent evidence indicates that long non-coding RNAs are dysregulated in a variety of cancers including EAC. In this study, siRNA mediated gene knockdown, Western blot, RT-PCR, as well as oncogenic function assay were performed. We found that the cell proliferation, colony formation, invasion and migration were decreased after LINC00857 knockdown in EAC cell lines. We also found that knockdown LINC00857 could induce apoptosis. Mechanistically, we found that the MET, STAT3, c-Myc and p-CREB proteins were decreased after LINC00857 knockdown. Our study suggests that LINC00857 may play an important oncogenic role in EAC via STAT3 and MET signaling.
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