Breast Cancer Metabolism Research


Identifying Mitochondrial Determinants in Breast Cancer Control and Translating Fundamental Research Discoveries to Clinical Utility

Mitochondria are the key bioenergetic organelles that integrate the three major sources of metabolic nutrients (carbohydrates, amino acids and lipids) and harness the bioenergetic capacity to sustain energy metabolism in every living cell. Mitochondria serve two critical roles in cellular homeostasis: namely, adenosine triphosphate (ATP) generation and programmed cell death (intrinsic apoptosis). Aberrant mitochondrial function has been implicated in a variety of metabolic disorders, including diabetes, obesity and cancer. Our laboratory research efforts are centered at the interfaces of mitochondrial biology and breast cancer metabolism.


Figure 1: Normal cells have controlled orchestration of growth factor signaling pathways and cell cycle control networks. Aberrations in one or more of these components lead to cancer; our research is focused on the role of mitochondrial function in modulating these critical cancer-associated signaling pathways.

Figure 2: Schematic of how impairments in mitochondrial complex I function can lead to a cascade of metabolic deficits promoting/sustaining cancer growth in animal models and human patients.

Figure 3: Representative images of 3-D mammary epithelial spheroids labeled with mitochondrial membrane potential marker, hypoxia marker (carbonic anhydrase 9), cell proliferation marker (Ki-67), mitochondrial matrix marker (complex II subunit) and nuclear marker (DAPI). We are developing tools to obtain functional correlation between tumor heterogeneity, tumor cell proliferation and mitochondrial function in 3-D architectures.

Figure 4: Representative image showing single-cell resolution imaging in whole mouse mammary gland (approximately 500 microns thick) cleared and labeled with epithelial cell surface marker beta-cateni.

Collaborative Research

Representative Publications

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