Cells have many activities - they grow, they divide, they secrete and they die. Our laboratory studies the process of cell death (apoptosis is a more specific name for programmed cell death). Defects in apoptosis can lead to development of a number of diseases, such as cancer, autoimmunity and neurodegeneration. At the center of apoptosis is a set of enzymes known as caspases. During apoptosis, they become active and orchestrate the death of the cell. One mechanism of caspase activation involves the release of cytochrome c and other apoptosis-inducing factors from damaging mitochondria. Now, it is clear that mitochondrial membrane permeabilization (MMP) is a near-to-universal feature of early cell death and loss of the mitochondrial transmembrane potential becomes a hallmark of apoptosis. We can use this interesting feature to screen drugs. Our laboratory is interested in elucidating the molecular mechanisms of apoptosis, i.e., how cells die, why they die and how to prevent or promote cell death. In particular, we are interested in elucidating how mitochondria regulate the apoptosis in 'normal' and drug-resistant cancer cells. We are wondering how the resistance of mitochondria to MMP can explain the resistance of cancer cells to apoptosis induction, and we hope to develop strategies for overcoming chemotherapy resistance by targeting tumor mitochondria. For example, we are evaluating several cytotoxic compounds from Chinese medicinal herbs with direct action on mitochondria. We believe that pharmacological interventions on mitochondria are good strategies to promote cell death in tumor cells. This research topic on apoptosis is therefore relevant to disease treatment with socioeconomic impacts.