Division of Cancer Cell Biology
Laboratory Web site
TAKEUCHI, Yasuto （Young PI）
Aims, Ongoing Projects, and Recent Achievements
Our major research interest is to elucidate the molecular mechanisms regulating cancer cells, stem cells and cancer stem cells. Our team has two important research directions: One is to clarify the basic principles underlying biology and the other is to apply the knowledge extracted from the basic principles to translational medicine. In order to achieve the goal, we take challenging approaches of molecular biology and systems biology, in addition to conventional methods of molecular biology.
- Molecular mechanisms of cancer initiation, progression and metastasis: breast cancer stem cells as key players
By analyzing the mouse cancer model or primary cancer cells derived from human specimens, we attempt to identify novel molecular targets and biomarkers for cancer. We are collecting breast cancer patient samples and culturing them as spheroids and organoids and constructing patient-derived xnograft models (PDXs).
- Analysis of mitochondrial metabolic pathways in cancer cells
“One carbon metabolism” in which one carbon derived from serine is activated specifically in cancer cells. We have found that the one carbon metabolism is not only used for de novo synthesis of DNAs or RNAs but also for maintenance of cancer stem cells. Furthermore, these enzymes are promising molecular targets for cancer therapy.
- Signal transduction mechanisms through receptor tyrosine kinases (RTKs) for tumorigenesis and stem cell maintenance
Fibroblast growth factor (FGF) and epidermal growth factor (EGF) RTKs play major roles for a variety of physiological and pathological aspects of biology, including stem cell biology, and cancer biology. We focus on FRS2 family of adaptor/scaffolding docking proteins, as key intracellular signal regulators of these RTKs.
The most prevalent cancer globally, breast cancer develops from premalignant conditions. It is highly desirable to prevent breast cancer from developing by finding ways to treat these premalignant conditions. But the molecular mechanisms behind them are not well understood. We have discovered that the adaptor protein FRS2β triggers changes in the cellular microenvironment that give rise to premalignant conditions in mice. Specifically, we found that FRS2β creates a microenvironment that has a high concentration of cytokines for promoting tumorigenesis.