Cell Cannibalism as Cancer Defense!

https://doi.org/10.7554/eLife.27134.001A new study suggests that the mysterious process by which one cell consumes another may be triggered by cell division, potentially helping to fight tumor growth.

Jef Akst, The Scientist, 2017


This time-lapse video captures the process of cell cannibalism, or entosis, in which one cell engulfs another.BABRAHAM INSTITUTE

Watching the process of cell cannibalism using time-lapse microscopy, researchers have discovered new clues as to how and why cells may resort to eating one another. The team found that human epithelial cells, at the root of more than 80 percent of human cancers, can be triggered to cannibalize another cell following division, especially if the dividing cells, which normally remain rooted to their biological substrate, start to detach.

The results suggest that the cannibalistic process, also known as entosis, might slow cancerous growth, as “normal epithelia may engulf and kill aberrantly dividing neighbours,” the researchers write in the study, published today (July 11) in eLife.

“We set out to identify the proteins that control cell cannibalism in tumour cells, but by using time-lapse microscopy to watch this process in action, we stumbled across a completely unexpected new mechanism,” Jo Durgan of the Babraham Institute in Cambridge, U.K., says in a press release. “The link we’ve found to cell division is really intriguing from the perspective of cancer.”

“Entosis is a fascinating process that may play a role in normal physiology, as well as cancer,” adds the Babraham’s Oliver Florey. “After 100 years of observing ‘cell-in-cell’ structures, there is now an exciting push towards discoveries in both cell and cancer biology.”

Mitosis can drive cell cannibalism through entosis

eLife 2017;6:e27134 DOI: 10.7554/eLife.27134

Entosis is a form of epithelial cell cannibalism that is prevalent in human cancer, typically triggered by loss of matrix adhesion. Here, we report an alternative mechanism for entosis in human epithelial cells, driven by mitosis. Mitotic entosis is regulated by Cdc42, which controls mitotic morphology. Cdc42 depletion enhances mitotic deadhesion and rounding, and these biophysical changes, which depend on RhoA activation and are phenocopied by Rap1 inhibition, permit subsequent entosis. Mitotic entosis occurs constitutively in some human cancer cell lines and mitotic index correlates with cell cannibalism in primary human breast tumours. Adherent, wild-type cells can act efficiently as entotic hosts, suggesting that normal epithelia may engulf and kill aberrantly dividing neighbours. Finally, we report that Paclitaxel/taxol promotes mitotic rounding and subsequent entosis, revealing an unconventional activity of this drug. Together, our data uncover an intriguing link between cell division and cannibalism, of significance to both cancer and chemotherapy.


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