Resolving the Signaling Events that Control Cancer Invasion
The Mendoza laboratory strives to understand the biochemical signals that drive cell motility and the consequences of their activation during cancer progression.
Cell motility is essential to embryogenesis, immune response, wound healing, and cancer metastasis. During this process, iterative cycles of edge protrusion and retraction, adhesion to the extracellular matrix, and cell body contraction propel cells forward. The distinct motility structures and steps are mechanistically coupled and their dynamics are temporally coordinated. Control is mediated by physical forces and chemical signals.
Questions in the Mendoza lab span the range of fundamental investigation into mechanisms of cytoskeleton control and modeling cancer invasion and metastasis in vivo:
How do biochemical signals coincidently alter the strength and timing of distinct cytoskeletal dynamics to promote movement?
How do cancer mutations alter 3D cell morphology and enable invasion through altered tumor microenvironments?
In cancers with KRAS and BRAF driver mutations, does ERK/RSK signaling promote invasion and what “sweet-spot” level of signaling is needed?
The Mendoza lab has a funded collaboration with the Snyder lab to investigate the signaling mechanisms that contribute to ERK hyper-activation and tumor progression in KRas positive, Nkx2.1 negative lung cancers. This project is jointly carried-out by Rediet Zewdu and Kelley Ingram.
