Mendoza Lab
Mendoza Lab
Biochemical Signals and Physical Forces in Cancer Cell Invasion
The Mendoza lab endeavors to understand the fundamental signals that cause cells to migrate and invade and how signal activation can be avoided or targeted to improve lung cancer outcome. We work within an academic culture of learning and scientific integrity, empowering lab members to make an impact in cancer care through experimental discovery in cell and cancer biology.
Cell migration is essential to immune response, wound healing, and cancer metastasis. During this process, iterative cycles of edge protrusion, adhesion, and cell body contraction propel cells forward. These cellular structures that produce migration are mechanistically coupled and their dynamics are temporally coordinated. In cancer, mutations within the cancer cells or and changes in the tumor microenvironment create new chemical and biophysical signals that promote cancer cell movement. Deducing the molecular mechanisms of cell migration and cancer invasion will reveal new biomarkers and targets to predict and prevent cancer progression.
Cells use signaling pathways to continuously sense, integrate, and adapt to their environment. In lung cancer, the #1 cancer killer in the U.S., cell invasion occurs in the earliest stage I lesions. We study the signaling pathways that are mutated in lung cancer and the interactions between tumor cells and the physical forces and extracellular matrix in the tumor microenvironment. Our questions span fundamental investigation into the mechanisms of cytoskeleton control and in vivo cancer invasion and metastasis. We combine live-cell imaging and computer vision with mouse models with computational modeling to understand the mechanisms of cell migration and tumor cell interactions with the microenvironment.
- How do biochemical signals synergistically regulate actin, adhesion, and membrane dynamics for cell movement?
- How does altered extracellular matrix in the tumor microenvironment promote early cancer invasion and progression?
- How does amplified strain in across diseases lung tissue contribute to tumor growth?
Affiliations
- Department of Oncological Sciences
- Department of Biomedical Engineering
- Cancer Biology and Microenvironment Program
- Lung Center of Excellence
- Computational Oncology Research Initiative
- Molecular Biology Graduate Program
Collaborations
Mechanobiology: The Mendoza lab has a funded collaboration with the Weiss lab in the Biomedical Engineering department. This collaboration applies computational modeling and experimental stretching of lung tissue to understand the biomechanical signals involved in lung tumor growth.
Pollution and lung cancer: The Mendoza has lab a funded collaboration with Drs. Judy Ou and Chen Chen in Population Health Sciences to understand and target the cancer-promoting signals in particulate matter pollution.
Pathology: Support is also provided by Dr. Lyska Emerson in the Department of Pathology.
