Dustin 

10-20% of breast cancer cases are a subtype called Triple Negative Breast Cancer (TNBC).  In TNBC, the overexpression of two proteins, PARP1 and NCL, is related to its resistance to conventional chemotherapy drug treatment. PARP1 supports cancer cell survival by detecting DNA damage and coordinating repair mechanisms through binding to any exposed ends of the DNA. This maintains cancer cell structure, allowing for repair. NCL, on the other hand, promotes cancer cell survival by stabilizing mRNAs in the nucleus. Past research has shown that silencing PARP1 in pancreatic cancer has led to suppressed growth and cell progression. This was done through treating pancreatic cancer cells with PARP1-siRNA, an siRNA that silences PARP1. In addition, it has been found that inhibiting PARP1 can lead to higher sensitivity to some chemotherapies in melanoma cells, reflecting promise across cancer types. The goal of this project is to silence PARP1 through the use of PARP1-siRNA-1706 in TNBC cells in vitro treated with docetaxel, a form of chemotherapy, and to analyze the DNA damage in response. If the results demonstrate reduced resistance to treatment, this approach could be used in future TNBC treatments.