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Emily Ho
Associate Professor, Nutrition and Exercise Sciences
Principal Investigator, Linus Pauling Institute
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RESEARCH:
My research focuses on understanding the molecular mechanisms by which antioxidant nutrient status affects the initiation and/or progression of chronic disease states such as cancer. Low intake of several antioxidant nutrients, such as zinc could be major risk factors for several types of cancer, as suggested by both epidemiological and laboratory studies. My work suggests that compromised antioxidant status not only increases oxidative damage to DNA, but also affects signal pathways resulting in dysregulation of repair and growth in cells. The overall goal of my research is to identify the molecular mechanisms by which antioxidant status affects DNA integrity and cancer development. There are several areas of interest in the laboratory:
1) Zinc, oxidative stress and DNA integrity: Zinc is a component of over 300 proteins, including DNA-binding proteins with zinc fingers, Cu/Zn superoxide dismutase and several proteins involved in DNA repair, such as p53, which is mutated in half of human tumors. It can be hypothesized that insufficient zinc intake will impair antioxidant defenses and compromise DNA repair mechanisms, making the cell highly susceptible to oxidative DNA damage. Thus, deficits in zinc intake could also have a major impact on an individual’s stress response and risk for developing cancer. In the laboratory we are identifying molecular mechanisms by which zinc acts as an antioxidant and protects us from environmental challenges.
2) Zinc and prostate cancer: A significant portion of the population is at risk for marginal zinc deficiency and potential risk for cancer. The prostate contains the highest of concentration of zinc in the body and is sensitive to zinc fluctuations. However, the function of zinc in the prostate remains unknown. Low zinc intake could dramatically increase one’s risk for developing prostate cancer. Zinc acts to combat against oxidative damage, plays a role in DNA repair and also bears important anti-inflammatory and anti-proliferative properties. Zinc deficiency has also shown to compromise reproductive & hormonal function in men and zinc metabolism declines with age. We expect that zinc supplementation would be highly effective in limiting prostate cancer by limiting oxidative stress, enhancing DNA repair and inhibiting inflammation and proliferation. The ability of zinc to target multiple points of the carcinogenic pathway and its unique importance in the prostate could make zinc an effective chemoprevention agent. This proposal will establish the mechanistic role of zinc in the development of prostate cancer in both in vitro and in vivo models.
3) Identification of zinc status biomarkers: Currently a reliable marker for zinc status does not exist. Using genomic and molecular approaches we are probing for novel markers for zinc deficiency in humans.