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Sci. Signal., 11 February 2014
Vol. 7, Issue 312, p. pc5
Science Signaling Podcast: 11 February 2014
Erik H. J. Danen1,2 and
Annalisa M. VanHook2
1 Division of Toxicology, Leiden Amsterdam Center for Drug Research, Leiden University, Leiden 2333C, Netherlands. 2 Web Editor, Science Signaling, American Association for the Advancement of Science, 1200 New York Avenue, NW, Washington, DC 20005, USA.
This Podcast features an interview with Erik Danen, author of a Research Article that appears in the 11 February 2014 issue of Science Signaling, about how interfering with cell adhesion signaling through the cell surface receptor β1 integrin affects the behavior of triple-negative breast cancer (TNBC) cells. Contacts with neighboring cells and with the extracellular matrix are very important in controlling the growth, survival, and behavior of epithelial cells. Loss of cell contacts can trigger extrusion of epithelial cells and subsequent apoptosis. The epithelial-to-mesenchymal transition (EMT) is a process by which epithelial cells leave the epithelial sheet and become migratory instead of undergoing apoptosis. EMT occurs as a normal part of development, but EMT also occurs in cancers, where it can drive metastasis. Integrins are cell surface receptors that mediate interactions between cells and between cells and extracellular matrix. Signaling through integrins promotes survival and proliferation, so drugs that block integrin-mediated signaling are candidates for cancer therapeutics that could be used to kill epithelial cell cancers. Truong et al. report that TNBC cells lacking β1 integrin produced smaller tumors when injected into mice but were more metastatic than TNBC cells with β1 integrin.
Citation: E. H. J. Danen, A. M. VanHook, Science Signaling Podcast: 11 February 2014. Sci. Signal.7, pc5 (2014).
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