The medicinal use of
aspirin stretches back to ancient times, before it was manufactured in its pure form in the late 19th century. Its accepted mechanistic target,
cyclooxygenase (COX), was discovered in the 1970s and since this landmark discovery, the therapeutic application of
aspirin and other non-steroidal anti-inflammatory drugs (
NSAIDs) has increased dramatically. The most significant benefits of
NSAIDs are in conditions involving chronic
inflammation (CI). Given the recognized role of CI in
cancer development, the use of long-term
NSAID treatment in the prevention of
cancer is an enticing possibility. COX-2 is a key driver of CI, and here we review COX-2 expression as a predictor of survival in various
cancer types, including breast.
Obesity and post-partum involution are natural inflammatory states that are associated with increased
breast cancer risk. We outline the COX-2 mediated mechanisms contributing to the growth of
cancers. We dissect the cellular mechanism of epithelial-mesenchymal transition (EMT) and how COX-2 may induce this to facilitate
tumor progression. Finally we examine the potential regulation of COX-2 by c-Myb, and the possible interplay between c-Myb/COX-2 in proliferation, and
hypoxia inducible factor-1 alpha (HIF1α)/COX-2 in invasive pathways in
breast cancer.