Summer Research Description: Breast cancer metastasis is a major issue for cancer patients. As tumor cells spread, they ultimately change themselves to adapt to the microenvironment, causing relapses in cancer patients. In recent years, the role of chemokines and receptors have been studied in metastasis. It has been shown that the expression of certain chemokines and/or their receptors can entrain neutrophils to kill tumor cells. We hypothesize that increasing the levels of chemokines (CCL2, CXCL12, and CXCL1) and/or reduction of TGFβ can increase neutrophil killing to stop metastasis.
In this project, we will be looking at highly metastatic (4T1) and poorly metastatic (67 NR) cancer lines in BALB/c mice. We will assess neutrophils killing using reporter assays to measure the amount of tumor cells killed by neutrophils. ROS assays will be utilized to measure the amount of reactive oxygen species created by neutrophils to kill tumor cells. Finally, using enzyme-linked immunosorbent assays (ELISAs) we will measure the concentration of chemokines present in culture media samples. We hope gain insight into the role of chemokines and their receptors in breast cancer metastasis. Ultimately, we hope to improve treatment regimens by adding chemokines and/or TGFβ antagonists to existing therapies in order to reduce metastasis and mortality.