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| A human breast cancer cell, adenocarcinoma MDA-MB-231, demonstrates metastatic-like adhesion, spreading and migrating in a collagen matrix designed to mimic soft tissue. New research led by Penn State reveals for the first time the mechanics behind how breast cancer cells may invade healthy tissues. The discovery, showing that a motor protein called dynein powers the movement of cancer cells in soft tissue models, offers new clinical targets against metastasis and has the potential to fundamentally change how cancer is treated. Image Credit: Erdem Tabdanov / Pennsylvania State University (CC BY-NC-ND 4.0 DEED) |
The most lethal feature of any cancer is metastasis, the spread of cancer cells throughout the body. New research led by Penn State reveals for the first time the mechanics behind how breast cancer cells may invade healthy tissues. The discovery, showing that a motor protein called dynein powers the movement of cancer cells in soft tissue models, offers new clinical targets against metastasis and has the potential to fundamentally change how cancer is treated.
“This discovery marks a paradigm shift in many ways,” said Erdem Tabdanov, assistant professor of pharmacology at Penn State and a lead co-corresponding author on the study, recently published in the journal Advanced Science. “Until now, dynein has never been caught in the business of providing the mechanical force for cancer cell motility, which is their ability to move themselves. Now we can see that if you target dynein, you could effectively stop motility of those cells and, therefore, stop metastatic dissemination.”
The project began as a collaboration between Penn State’s Department of Chemical Engineering and Penn State’s College of Medicine, before growing into a multi-institution partnership with researchers at the University of Rochester Medical Center, Georgia Institute of Technology, Emory University, and the U.S. Food and Drug Administration.






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