The main interests of our lab are aging and age-dependent cancer risk. In particular, we are interested in the biological functions of senescence in aging, stem cell self-renewal and oncogenesis. Senescence, a process in which cells stop dividing, is regarded as an antagonistic pleiotropy in cancer and aging. By limiting cell proliferation, senescence may lead to the decline or even depletion of the self-renewal capacities of stem or progenitor cells, which interferences with normal tissue homeostasis and ultimately contributes to aging. On the contrary, senescence can be beneficial to organisms as it functions as a tumor suppressor to restrict the proliferation of cells at risk of malignant transformation. The complexity of the relationship between aging and cancer will be explored using knockout and transgenic mouse models, in which senescence response is modulated in vivo. In addition, efforts are directed at elucidating the genetic pathways of senescence and molecular targeting of transcriptional factors by the Nedd4 family of E3 ubiquitin ligases.