Cancer is the uncontrolled division of abnormal cells in a tissue. According to the American Cancer Society about 1 in 8 women in the United States will develop invasive breast cancer during their lifetime, making breast cancer the most common cancer among American women,except for skin cancers (American Cancer Society, 2013). With growing cases in the United States, cancer prevention may be the best means of reducing breast cancer mortality. One means of preventing breast cancer is daily aspirin treatment. According to a number of recent studies, including one by Rothwell and colleagues (2011), daily aspirin is implicated in cancer prevention. Aspirin is a commonly used Non-Steroidal Anti-Inflammatory Drug (NSAID). Although these studies suggest that aspirin may prevent cancer related death the molecular mechanism of this is unknown. The best known mechanism of action of aspirin is the inhibition of cyclooxygenase or COX enzymes. COX enzymes transform free arachidonic acid into the precursor prostaglandin (PG), PGH2. Specific synthases convert PGH2 into the bioactive molecules thromboxane (TXA2), PGI2, PGD2, and PGF2α. According to Schneider and colleagues (2011) PGs can promote and/or inhibit tumor growth. However, the mechanisms by which PGs regulate cancer are largely unknown. To address this knowledge gap, the Tootle lab has been utilizing Drosophila. These studies have revealed that PG regulates the actin bundling protein Fascin. Fascin levels correlates with aggressive tumors and Fascin implicated to promote invasion. This leads us to hypothesize that PGs promote cancer by regulating Fascin. Here we will assess whether aspirin has a dose dependent effect on Fascin expression.