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

p>Scheel notes that these experiments show how cancer cells' knack for usurping normal cell functions could ultimately lead to their downfall.

"These autocrine signals are not something breast cancer cells invent anew, but derive instead an activation of normal stem cell programs," says Scheel. "Breast cancer stem cells rely on these signals to maintain themselves, so they remain susceptible to blocking this autocrine signaling. It might be a terrific way to target breast cancer stem cells. In addition, our gain in understanding how both migratory and self-renewal traits are activated in normal breast epithelial cells might further our understanding of normal tissue homeostasis and might be of great utility in the area of regenerative medicine, where it would be highly desirable to create great numbers of epithelial stem cells without resorting to genetic intervention."

Although Scheel's research gives new insight into how both cancer and normal breast cells transition to and maintain a mesenchymal cell state, she and Weinberg caution that the same signals and signaling pathways may not apply for non-breast cells.

"Are the same agents signaling the EMT in non-mammary tissues the skin, liver, the gut, pancreas and so forth? We don't know the generalizability of Scheel's findings yet, although I can imagine that there are many commonalities," says Weinberg, who is also a professor of biology at MIT and the Director of the MIT/Ludwig Center for Molecular Oncology. "Secondly, we don't know if these three signaling pathways are ultimately those that are critically important for activating the EMT in non-mammary cell types. Alternatively, there may be other contextual signals besides these three that play an equally important role in triggering an EMT in non-mammary cells? Whether these signaling pathways turn out to have a degree of universality, we just don't know."


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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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