This investigation aims to gather foundational knowledge for harnessing viral genes to combat cancer cell resistance to traditional cancer therapies such as radiation and chemotherapy. Our study asks if it is possible to improve the cancer-killing capacity of drugs like etoposide by inactivating cellular proteins that cause resistance to chemotherapy through activation of DNA repair. Adenovirus targets DNA repair proteins naturally during infection to overcome intrinsic host cell defenses and promote a productive infection. By expressing viral genes in cancer cells, it may be possible to increase their vulnerability to chemotherapy or radiation treatment. Experiments were conducted with the A549 non-small cell lung cancer cell line isolated from a male lung cancer patient. Cells were treated with either a chemical inhibitor for a DNA repair protein, a chemotherapy agent, or both, and several assays were performed to assess the survivability of cells following these treatments. Western blotting was also used to identify individual DNA repair proteins in cell samples to determine the effect of treatment on their expression and activation. The results demonstrated an increase in the proportion of cancer cells dying when using combined treatments of both chemical inhibitor and chemotherapy drug rather than using them individually. More work is required to see if this effect is achievable using viral gene products rather than chemical inhibitors. Future studies will survey more cancer cell lines and begin the construction of vectors to deliver viral genes to cancer cells to observe their impact on the response of these cells to chemotherapy. Taken altogether, this experience has helped me engage with the scientific process, develop hypotheses and analyze data critically to draw conclusions, skills that I will continue to rely on during my graduate studies.
Author: Gabriel Ortiz
Faculty Advisor: Eileen Bridge, Microbiology
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