期刊
ONCOLOGY REPORTS
卷 37, 期 6, 页码 3590-3596出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/or.2017.5614
关键词
MCM7; proliferation; migration; AKT1; mTOR
类别
资金
- National Natural Science Foundation of China [81460425]
- Yunnan Provincial Research Foundation for Basic Research, China [2013FD012]
- Foundation for the Talents of Kunming University of Science and Technology [KKSY201226099]
The roles and mechanisms of mini-chromosome maintenance complex component 7 (MCM7) amplification and overexpression in esophageal carcinogenesis were investigated. By analyzing the TCGA datasets, we found that MCM7 was amplified in approximately 12% of esophageal squamous cell carcinomas (ESCCs), and in more than 4% of head and neck squamous cell carcinomas and stomach carcinomas. Overexpression of MCM7 was further verified in three independent GEO datasets of esophageal cancer. Knockdown of MCM7 using two siRNAs significantly inhibited cell proliferation, colony formation and migration of KYSE510 and EC9706 cells in vitro. Noteworthy, we further found that silencing of MCM7 suppressed the phosphorylation of AKT1 and mTOR both in KYSE510 and EC9706 cells, and reduced the cell cycle regulatory proteins cyclin Dl, cyclin E2 and CDK2. Taken together, our findings suggested that MCM7 promoted tumor cell proliferation, colony formation and migration of ESCC cells via activating AKT1/mTOR signaling pathway.
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