Journal
CELL RESEARCH
Volume 24, Issue 11, Pages 1288-1298Publisher
INST BIOCHEMISTRY & CELL BIOLOGY
DOI: 10.1038/cr.2014.137
Keywords
entosis; cadherin; Rho GTPase; actomyosin; p190A RhoGAP; tumor suppression
Categories
Funding
- NCI [CA154649]
- NIGMS [GM09312]
- Geoffrey Beene Cancer Research Center at MSKCC
- Louis V Gerstner, Jr Young Investigators Fund
- Benjamin Friedman Research Fund
- National Basic Research Program of China [2015CB553704]
- National Natural Science Foundation of China [30871364, 81472588]
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Cell engulfment typically targets dead or dying cells for clearance from metazoan tissues. However, recent evidence demonstrates that live cells can also be targeted and that engulfment can cause cell death. Entosis is one mechanism proposed to mediate the engulfment and killing of live tumor cells by their neighbors, an activity often referred to as cell cannibalism. Here we report that the expression of exogenous epithelial cadherin proteins (E- or P-cadherin) in human breast tumor cells lacking endogenous expression of epithelial cadherins induces entosis and inhibits transformed growth. Entosis induced by cadherin expression is associated with the polarized distribution of Rho and Rho-kinase (ROCK) activity within entotic cells, which is dependent on p190A RhoGAP activity. ROCK inhibition or downregulation of p190A RhoGAP expression reduces entosis and increases the transformed growth of epithelial cadherin-expressing tumor cells. These data define new cell systems for the study of entosis, and identify entosis as a mechanism of cell cannibalism that is induced by the establishment of epithelial adhesion and inhibits transformed growth.
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