Abstract
Analysis of oxidative stress and cytochrome c release in the presence of chemotherapy treatments will help further understand the mechanism by which apoptosis is promoted in cancer cells. The Bcl-2 family plays a significant role in regulating apoptosis in the cell. Bak and Bax are two of the most important pro-apoptotic proteins within this family as they are responsible for forming a pore in the mitochondrial outer membrane that regulates the release of cytochrome c. Determining how chemotherapy treatments, such as etoposide, taxol, and cisplatin, target this pore and result in cytochrome c release and subsequent generation of reactive oxygen species will help in directing avenues for future research to create more effective treatments. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. The inhibition of topoisomerase II prevents DNA from unbinding, an action required for replication, prompting apoptosis in cancer cells. Taxol works to stabilize the microtubules which are involved in many specific cellular functions regarding cell division. Stabilization works to prevent mitosis; this causes the cell cycle checkpoint to halt cellular proliferation. Cisplatin is the final drug being investigated; its role is to form crosslinks in DNA, disrupting the strands and inhibiting replication. The similarities and differences of these three chemotherapy drugs are important to explore. Understanding how the different mechanisms of chemotherapy treatments lead to mitochondrial mediated apoptosis will help in evaluating drug targets for future research.