Welcome to the Faubert Lab!
Metabolism is at the core of nearly every biological function. Alterations in proper metabolic function or control contribute to numerous diseases. In cancer, alterations of metabolic flux are a defining characteristic as they support cell growth and survival of malignant cells.
The Faubert lab seeks to understand metabolic rewiring in cancer, and how these altered metabolism contributes to disease progression. The lab utilizes mass spectrometry-based platforms, isotope tracers, and flux analysis to dissect the metabolic programs that underlie key malignant features. This work spans the areas of cancer metabolism, the tumor microenvironment and immunometabolism. Ultimately, we aim to utilize our findings for clinical benefit, as alterations in tumor cell metabolism can be leveraged into new therapeutic strategies, imaging techniques, and biomarkers.
Research Focus
Check out some of the work we do!
- Metabolism In Vivo/Isotope Tracing
- Metabolism and Metastasis
- Cancer Metabolism in Unique Microenvironments
Cancer cell metabolism is influenced by both internal (cell type, mutation status) and external (microenvironment, cell-cell interactions, nutrient availability) factors. To advance our understanding of altered tumor metabolism, our research incorporates both cell culture and in vivo models to analyze tumor biology. The laboratory has extensive experience in measuring metabolism in vitro and in vivo, including measuring tumor metabolism intra-operatively in patients. The laboratory utilizes a series of mass spectrometry platforms to provide comprehensive views of metabolic pathways in biological systems. We use a variety of methods to assess metabolism, including isotope tracing (13C, 2H, etc.), metabolomics, and metabolic flux to dissect the metabolic programs that underlie these key malignant features.
Not all tumors metastasize. This begs the question- what makes aggressive tumors different? What unique capabilities are inherent in these cancer cells that allow them to spread to distant organs? One contributing factor is the underlying metabolic differences between aggressive and non-aggressive tumors. Identifying the metabolic features that predict aggressive tumor behavior is an important prognostic and therapeutic biomarker. If we target these differences therapeutically, can we limit metastasis?
To study metastasis, the lab utilizes unique, patient-derived xenografts derived from clinical studies of primary human lung cancer. These PDXs match the metabolic phenotype of the primary tumor and spontaneously metastasize in mice, providing a tractable model to evaluate the role of metabolism in promoting and driving metastatic features, and what molecular characteristics underlie these phenotypes.
Cancer cells can be remarkably adaptable. While some metabolic processes are maintained in any environment, other pathways can be significantly affected by the tumor location. A clear example of this is the diverse and stage-specific metabolic challenges that occur during the metastatic cascade. These differences may have significant implications for imaging and therapy, but we first need a more comprehensive understanding of these tissue-specific adaptations.
To address this, the Faubert lab is developing new imaging and metabolic techniques to assess tumor metabolism in vivo. We utilize stable isotope tracers, a rapidly evolving approach that is currently the only method to measure metabolic activity in vivo. Isotopically labeled metabolites are safe, non-radioactive tracers that can label metabolic pathways in physiological concentrations, and have been used effectively in both animal models and patients. We are combining these tracer techniques with rapid cell isolation assays, to measure metastatic tumors in different organ locations.
