Journal
JOURNAL OF MAMMARY GLAND BIOLOGY AND NEOPLASIA
Volume 20, Issue 3-4, Pages 109-119Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10911-015-9333-4
Keywords
COX-2; Chronic inflammation; c-Myb; Breast cancer; EMT; HIF1 alpha
Categories
Funding
- EMPathy National Collaborative Research Program - National Breast Cancer Foundation, Australia
- National Health and Medical Research Council (NHMRC) [1027527]
- Raine Foundation at the University of Western Australia
- NHMRC
- Victorian Government's Operational Infrastructure Support Program
- Peter MacCallum Cancer Institute
- National Breast Cancer Foundation [CG-10-04] Funding Source: researchfish
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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 (HIF1 alpha)/COX-2 in invasive pathways in breast cancer.
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