Tel: 313-577-9433; Fax: 313-577-9469
Department of Pathology,Integrated Biosciences Bldg., Room 417
6135 Woodward Avenue
Detroit MI 48202
Administrative ContactMs. Brenda Batts, 313-577-1102
Our research seeks to understand metabolic requirements for embryonic stem cell (ES) self-renewal, and contribution of aberrant metabolism to cancer development. ES cells and cancer cells share some common properties, notably autonomy in proliferation and preference for glycolytic metabolism. The key regulatory mechanism of ES cells is often hijacked by cancer to gain “stemness”. Previously we found mitochondrial threonine degradation as an essential mechanism to sustain mouse ES cell self-renewal, wherein threonine is broken down into glycine and acetyl-CoA, which in turn fed into core anabolic/catabolic pathways via glycine cleavage system and TCA cycle. Given the similarities between the metabolism of ES and cancer cells, we hypothesize the aforementioned pathways could constitute a hot spot to promote cancer development. Our current research is to determine the role of mitochondrial threonine/glycine metabolism in pluripotency reprogramming and tumorigenesis. Also, we study towards identifying metabolic changes in epithelial to mesenchymal transition (EMT), a critical embryonic developmental process with important role in tumorigenesis.
M.D. (1989), Tongji Medical University, Wuhan, China