Self-repairing cancer cells future of cancer treatments

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ITHACA, N.Y. – With narrow bodies and no collarbones, mice are able to squeeze through holes as small as a quarter-inch in diameter.

Cancer cells similarly are able to migrate through extremely tight quarters but with a major difference: The journey often comes at a price – the deformation and, in some cases, rupture of the outer lining of a cell’s nucleus. While deformation and rupture can sometimes lead to cell death, the cell – about 90 percent of the time – also has the ability to repair itself.

A research group headed by Jan Lammerding, associate professor of biomedical engineering at Cornell University, has been studying this phenomenon in hope of using it to develop both treatment and diagnostic solutions for the millions of people who deal with cancer every day.

There is also the possibility that a ruptured cell could mutate into a more aggressive form of the disease.

“You have so many migrating cells,” Lammerding said, “that even if a small fraction of them picks up a mutation, it means the cancer is evolving. The good part is, this rupturing also makes the cancer cell vulnerable. Most cells in the body stay in place, and it’s presumably mostly cancer cells that are moving around. So if we can block the mechanisms that allow them to repair themselves, then we potentially could target metastatic cancer cells.”

The group looked at two factors in the cell’s migration process: the rupturing of the nuclear envelope, which they tracked using green and red fluorescent proteins normally localized to the cell nuclei, but that spill into the cell body when the nucleus ruptures; and damage to the cell’s DNA.

“We’re still trying to find out if there are differences between cells, and a lot of what we see is very similar between normal cells and cancer cells,” he said, adding that by trying to identify potentially unique deformation-and-repair properties of cancer cells, treatments that are minimally deleterious to healthy cells may be developed.

“Now that we kind of know what we’re looking for, now that we know the molecular pathways that these work in,” he said, “could we then specifically target invasive cancer cells and not have the sledgehammer that hits everything?”

Lammerding’s group reports on this research in a paper published online March 24 in First Release, from the journal Science.

This work was supported by grants from the National Institutes of Health, the Department of Defense Breast Cancer Research Program, the National Cancer Institute and the National Science Foundation.

Daryl Lovell
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