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Jul 8, 2014

Stopping Terminator-Style Cell Liquidity May Slow Cancer

Stopping Terminator-Style Cell Liquidity May Slow Cancer

By altering chemical signaling, it is possible to prevent cells from attaining an invasive, liquid-like state. In this image, cells are stained red for cell protrusion, yellow for cell membrane, and blue for nucleus. [Prof. R. Mayor, UCL]

  • If yet another film in the Terminator franchise were to released, it could depict John Connor struggling with a different kind of shape-shifting foe—a terminator within. Such an adversary, it turns out, may not be altogether fanciful. According to scientists at University College London (UCL), collections of cancer cells may adopt a liquid-like state, the better to slip though narrow channels in the body, flow from tissue to tissue, and ultimately wreak metastatic havoc.

    Of course, these cells don’t consist of a “mimetic polyalloy,” the liquid metal that made the T-1000 so formidable. Instead, the cells may simply loosen their links to neighboring cells, but not so much that they lose their ability to migrate collectively. To achieve this hybrid state—partly solid-like and partly liquid-like—cells respond to chemical signals.

    Chemical signals that can promote plasticity among cells have been detailed in an article by UCL researchers entitled “In vivo collective cell migration requires an LPAR2-dependent increase in tissue fluidity.” According to this article, which appeared July 7 in the Journal of Cell Biology, “the level of cell–cell adhesion is precisely regulated by internalization of N-cadherin downstream of lysophosphatidic acid (LPA) receptor 2.”

    To address the question of how cells that have downregulated cell–cell adhesions are capable of collective migration, the UCL researchers used neural crest cells, which rely on alteration of the cadherin repertoire to accomplish cell dissociation. These embryonic cells allowed the researchers to investigate how groups of cells move in a developmental process similar to that used by cancer to spread around the body.

    Using their model, the UCL researchers found that when membrane N-cadherin was reduced, the result was not, as one might expect, the generation of single, fully mesenchymal cells. Instead, it triggered a partial mesenchymal phenotype. The upshot is that cells that have gone through an epithelial-mesenchymal transition are still capable of collective cell migration. That is, these phenotypes, both common to cancer and morphogenesis, are not mutually exclusive.

    What’s more, when they switched off the signals from LPA, the scientists observed that the neural crest cells stopped moving down narrow, blood vessel-like channels.

    “We have found a way to stop the movement of embryonic cells by blocking LPA signals,” said lead scientist Professor Roberto Mayor (UCL Cell & Developmental Biology). “It is likely that a similar mechanism operates during cancer invasion, which suggests a promising alternative in which cancer treatments might work in the future, if therapies can be targeted to limit the tissue fluidity of tumors.”

    “Our findings are important for the fields of cell, developmental, and cancer biology,” Professor Mayor added. “Previously, we thought cells only moved around the body either individually or as groups of well-connected cells. What we have discovered is a hybrid state where cells loosen their links to neighboring cells but still move en masse together, like a liquid. Moreover, we can stop this movement.”


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