期刊
SCIENTIFIC REPORTS
卷 5, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/srep12223
关键词
-
资金
- National Basic Research Program of China [2015CB553704]
- National Major Scientific and Technological Special Project for Significant New Drugs Development [2015ZX09501-009]
- National Natural Science Foundation of China [81472588, 81273197, 81471578, 81371764]
- Pioneer Project for Young Scientist of Military Biomedicine [14QNP119]
- Pioneer Research Foundation
- Guangdong Province Universities and Colleges Pearl River Scholar Funded Scheme
- Beijing Municipal Natural Science Foundation [7142121]
- Beijing Institute of Biotechnology
Although cell-in-cell structures (CICs) could be detected in a wide range of human tumors, homotypic CICs formed between tumor cells occur at low rate for most of them. We recently reported that tumor cells lacking expression of E-and P-cadherin were incapable of forming homotypic CICs by entosis, and re-expression of E-or P-cadherin was sufficient to induce CICs formation in these tumor cells. In this work, we found that homotypic CICs formation was impaired in some tumor cells expressing high level of E-cadherin due to loss expression of alpha-catenin (a-catenin), a molecular linker between cadherin-mediated adherens junctions and F-actin. Expression of a-catenin in these tumor cells restored cell-cell adhesion and promoted CICs formation in a ROCK kinase-dependent way. Thus, our work identified a-catenin as another molecule in addition to E-and P-cadherin that were targeted to inactivate homotypic CICs formation in human tumor cells.
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