Cecilia Caino, PhD, has been researching cancer cell biology at University of Colorado Cancer Center since 2017. Cecilia earned her PhD in Cellular Biology from the University of Buenos Aires with her research component performed at the University of Pennsylvania, and completed a postdoctoral fellowship at The Wistar Institute. We spoke with Dr. Caino about her research on how cancer cells use energy and how their unique energy strategies could help cancer cells spread.

Cecilia Caino, PhD | University of Colorado Cancer Center
Cecilia Caino, PhD

What excites you most about your research?

Caino: I am a cell biologist at heart and I am curious to understand how and why cancer exploits structures called mitochondria for energy resources that allow cancer cells to spread and resist therapy. When you look at cells under the microscope, it is fascinating to see the constant dance of mitochondria, rushing about the cell and undergoing “kiss and go” cycles of fusion/division.

So how do cancer cells manipulate mitochondria?

Caino: Recently, we have learned that mitochondria don’t just stay in one place making energy. Instead, they use something called “mitochondrial dynamics,” which is the focus of my research: an individual mitochondrion can travel to different locations, fuse to another mitochondrion, or split into daughter mitochondria. We also see that mitochondria work with other structures inside our cells to promote cell fitness. These processes help healthy cells resist stress and adapt to changing environmental conditions. In cancer, reprogramming of mitochondrial dynamics helps cancer cells spread and resist therapy.

What convinced you that University of Colorado Cancer Center would be the best place to work on mitochondria research?

Caino: Much of what we know about mitochondrial dynamics was discovered in neurons, and we still have only limited knowledge of how they are wired in cancer. There are no drugs to target most of the processes of mitochondrial dynamics, and we don’t know what functions are crucial in cancer. As a Mentored Member of the CU Cancer Center and the Department of Pharmacology, I have access to outstanding collaborators and unparalleled resources to tackle some of these questions from basic cancer research, cell biology, structural biology and pharmacological angles.

How will your research impact the treatments being provided to cancer patients?

Caino: Our research is basic. We aim to identify how mitochondrial dynamics fuel metastasis. In the long term, this understanding may lead to drugs that can prevent or reduce cancer’s ability to spread.

What is the biggest breakthrough so far in your research?

Caino: We showed that cancer cells reprogram mitochondria to meet local demands for energy. Cancer exploits regional control of mitochondrial function, powering up mechanisms of invasion and metastasis.

What type of cancers will benefit the most from this research?

Caino: We have evidence that mitochondrial dynamics are dysregulated during metastasis of cancers including those of the prostate, breast, skin and brain. In animal models, we were able to block or reduce the spread of prostate cancer and melanoma by manipulating key players of mitochondrial dynamics. It is truly exciting to find differences between normal and cancer cells because this opens opportunities to target these differences in cancer cells and limit their metastatic potential.