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Resolving the Signaling Events that Control Cancer Invasion
Tumor spread and dissemination is the most significant cause of cancer morbidity and mortality. This spread is a cellular process, in which cancer cells become mobilized and invade out and away from the primary tumor site.
Cell motility is highly-orchestrated. A leading edge protrudes and adheres to the extracellular matrix, adhesions mature, the cell body contracts, and the back of the cell detaches. These morphological events are induced by mechanical changes in the actin and myosin cytoskeleton and cell adhesions. Our lab is dedicated to dissecting the molecular signaling events that control these mechanical changes.
How are structural changes in the cytoskeleton and adhesion structures regulated in spatially-restricted fashion across the cell? How is the power balanced and their timing sequenced to allow movement? And what happens in cancer, when mutations induce hyper-activation of these regulatory pathways?
To address these questions, our work spans the spectrum of in vitro biochemical studies, live-cell imaging with optogenetics, computational image analysis of cytoskeletal dynamics, and animal cancer models. By translating our fundamental mechanistic work into in vivo studies, we are uncovering the signals that control the aberrant motility of cancer cells during invasion and metastasis.