|Abstract or Summary
- Autophagy, a homeostatic degradation pathway, has a role in promoting cell survival under stress conditions, but can also promote cell death under conditions of sustained stress. This project investigates the cytotoxic potential of coibamide A and other natural products in autophagy-deficient and wild-type mouse embryonic fibroblasts (MEFs). Wild-type MEFs were more vulnerable to coibamide A than cells lacking autophagy-related protein 5 (Atg5). Through cell viability assays and immunoblotting for markers of autophagy, it was found that restoration of expression of Atg5, a vital autophagy-related protein, in an autophagy-null background was able to partially restore the response characterized in wild-type MEFs. These results lend support to the existence of crosstalk between autophagy and apoptosis, and suggest coibamide A as a compound with characteristics that may utilize autophagy for pro-death signaling.