Research Molecular Biologist
Dr. Zeng was born and grew up in Xiamen, China. He obtained B.S. and M.S. degrees in Biology from Xiamen University. He attended the University of Wyoming, where he earned a Doctor of Philosophy degree in Molecular Biology in 1996. After graduation, Dr. Zeng spent three and half years as a postdoctoral researcher at the National Institutes of Health investigating steroid hormone-induced gene expression. Dr. Zeng joined the scientific staff of the USDA-ARS Grand Forks Human Nutrition Research Center (GFHNRC) as a Research Molecular Biologist in November1999.
Obesity related colon cancer is a significant global health concern and the impact of specific dietary components on colon cancer risk has been well recognized. Dr. Zeng's main area of research is to determine the molecular mechanisms of cancer-preventive nutrients in foods. This focus presently centers on selenium-containing foods, and the development of new molecular bio-markers for obesity related colon cancer prevention. Currently, Dr. Zeng is studying the effects of nutritional levels of selenium in supporting cellular survival signaling; and the role of the putative anti-tumorigenic Se-metabolite, methylselenol, in cell cycle progression and apoptosis in both colon cell and animal models.
Dr. Zeng is also investigating the impact of human genetic variation on optimal nutritional intake. Single nucleotide polymorphisms (SNPs) are a primary component of human genetic variation. To determine the diet that best fits certain SNPs, He examines the effects of hemochromatosis, selenoproteins and vitamin D receptor genotypes on the absorption and utilization of iron, selenium, calcium and other nutrients.
Molecular Nutrition & Cancer Biology:
- Demonstrated for the first time that through the activation of certain pro-apoptotic genes linked to p53, NFkB, and stress signal pathways, mice fed a selenium-enriched broccoli had stronger apoptotic ability in response to spontaneous colon tumor development caused by a genetic defect. This contributes to our incomplete knowledge about how nutrients affect gene expression and reduce obesity-related cancer risk. The findings are important because sensitive gene markers are needed to evaluate the anticancer effect of functional foods.
- Demonstrated that both methylselenol and butyrate inhibit tumor cell migration and invasion, and that they exerted secondary cancer prevention through the inhibition of pro-MMP-2 activation. These findings provide the molecular evidence that secondary cancer prevention can be achieved by the high dietary intakes of selenium-enriched or high fiber foods. In addition, these data lay the ground work for screening sensitive gene markers that are needed to evaluate the anticancer foods such as selenium-enriched or high fiber foods.
- Demonstrated for the first time that an interaction between trace elements influences cell death signaling: (a) arsenic suppresses toxic necrosis induced by selenite. In addition, selenite inhibits cell death signaling induced by arsenic, and (b) copper directly interacts with selenite extracellularly to influence cell death signaling. This showed a mutual inhibition of cell death signaling by selenium and selenium-antagonistic elements. The findings provide the first molecular basis for the interaction between selenium and its antagonistic elements. The new knowledge is fundamental for determining the anti-cancer effects of dietary selenium and its requirement because the interrelationship of different trace elements must be taken into consideration for optimal biological function of selenium.
- Demonstrated for the first time that copper deficiency increases type I collagen content, DNA binding activity of a single-stranded cytosine-rich sequence, fibulin-5 (DANCE/EVEC) but decreases cytochrome C oxidase VIb subunit expression complex IV in the mitochondrial respiratory chain in rat heart using an extensive proteomic approach. These findings are particularly useful in facilitating the development of biomarkers regarding dietary copper status in human populations.