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Signaling pathways point to vulnerability in breast cancer stem cells
Date:6/9/2011

hat work together to maintain migratory and self-renewing traits of both normal breast epithelial and breast cancer cells. These pathways are continuously activated in the stem cells by autocrine signals; that is, signals produced by the cells themselves. Studying how these autocrine signals function in breast epithelial cells allowed Scheel to specify the signals that allow these cells to pass through an EMT and enter into a mesenchymal and stem cell-like state in the first place. Her findings are published in the June 10 issue of Cell.

Interestingly, Scheel discovered that epithelial cells are kept in their differentiation state via inhibition of the three signaling pathways, that is, normal epithelial cells naturally produce proteins that block these signaling proteins. To push normal breast epithelial cells through an EMT in vitro, she removed these endogenous inhibitors by administering a cocktail of neutralizing antibodies and added growth factors that stimulate the three pathways, thereby mimicking the autocrine signaling found in mesenchymal cells. By applying the resulting EMT-inducing cocktail continuously, Scheel pushed the cells into a mesenchymal and stem cell-like state, with associated increased migratory ability and stem cell-like characteristics. Eventually, the former epithelial cells stabilized this state through autocrine signaling and were no longer dependent on the EMT cocktail.

To see the effects of blocking this autocrine signaling in an animal model, Scheel implanted into mice human breast cancer epithelial cells that had passed through an EMT. She then injected the implantation site with proteins that block the three pathways. The injected mice had one-tenth the number of tumors found in mice that did not receive the inhibitory proteins. In addition, breast cancer cells that were pre-treated in vitro with these proteins displayed a greatly reduced ability to metastasize when subsequently implanted into mice.

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Contact: Nicole Giese
giese@wi.mit.edu
617-258-6851
Whitehead Institute for Biomedical Research
Source:Eurekalert

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