Current Research and Scholarly Interests
Hypoxia induces endoplasmic reticulum (ER) stress in solid tumors. Previous studies have indicated that hypoxia is a major determinant of local, regional, and distant recurrence after anticancer therapy. The response of tumor cells to hypoxia depends on the severity and duration of oxygen deprivation. For example, hypoxia induced factor (HIF-1) is activated at physiological levels of oxygen change, whereas the unfolded protein response (UPR) is induced by severe oxygen deprivation. The UPR is an evolutionarily conserved pathway that functions to reduce protein accumulation in the ER resulting in increased capacity to tolerate ER stress. We hypothesize that since the UPR is also activated during hypoxia, it may be a critical regulator of cell survival during hypoxia and is necessary for tumor growth. The focus of my laboratory is to understand the relationship between hypoxia and ER stress, particularly as it relates to tumorigenesis.