How we think and fall in love are controlled by lightning-fast electrochemical signals across synapses, the dynamic spaces between nerve cells. Until now, nobody knew that cancer cells can repurpose tools of neuronal communication to fuel aggressive tumor growth and spread. University of Texas (UT) Southwestern Medical Center researchers report these findings in two recent studies, one in PNAS and the second in Developmental Cell. The PNAS article (online January 3, 2017) is titled “TRAIL-Death Receptor Endocytosis and Apoptosis Are Selectively Regulated by Dynamin-1 Activation,” and the Developmental Cell article (online February 6, 2017) is titled “Crosstalk Between CLCb/Dyn1-Mediated Adaptive Clathrin-Mediated Endocytosis and Epidermal Growth Factor Receptor Signaling Increases Metastasis.” “Many properties of aggressive cancer growth are driven by altered cell signaling,” said Dr. Sandra Schmid, senior author of both papers and Chair of Cell Biology at UT Southwestern. “We found that cancer cells are taking a page from the neuron’s signaling playbook to maintain certain beneficial signals and to squelch signals that would harm the cancer cells.” The two studies find that dynamin1 (Dyn1) – a protein once thought to be present only in nerve cells of the brain and spinal cord – is also found in aggressive cancer cells. In nerve cells, or neurons, Dyn1 helps sustain neural transmission by causing rapid endocytosis – the uptake of signaling molecules and receptors into the cell – and their recycling back to the cell surface. These processes ensure that the neurons keep healthy supplies at the ready to refire in rapid succession and also help to amplify or suppress important nerve signals as necessary, Dr. Schmid explained. “This role is what the cancer cells have figured out.
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