Radiation Induced Apoptosis in 2LMP Breast Cancer Cells by Caspases and Mitochondrial Response

Undergraduate #18
Discipline: Biological Sciences
Subcategory: Cancer Research

Victoria Bates - Talladega College
Co-Author(s): Alison Brown, Talladega College, Talladega, AL

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Breast cancer is the second leading cause of death in women, exceeded only by lung cancer. Radiation to the breast is often
given after breast-conserving surgery to lower cancer recurrence in the breast or nearby lymph nodes. Apoptosis is a process of programmed cell death which plays a major role in a disease like cancer. The process of apoptosis is controlled by a diverse range of cell signals, which may originate either extracellularly (extrinsic inducers) or intracellularly (intrinsic inducers). Mitochondria play a central role in apoptotic signaling pathways. The focus of this study was to demonstrate apoptosis in radiated breast cancer cells by caspase initiation and mitochondrial dysfunction. Cell viability and cytotoxicity protease activity were measured and found not to be inversely proportional. Caspase activation showed a constant decrease as the radiation doses were increased. Biomarkers were used to assess mitochondrial integrity and ATP activity in the 2LMP breast cancer cells. The results showed a slight decrease in ATP activity as the doses increased. The decrease in ATP activity and caspase activation are indicative of apoptosis induction.

Funder Acknowledgement(s): Funding was provided by the United States Department of Education.

Faculty Advisor: Alison Brown,