Inflammation has become a research hotspot in solid tumours and has been confirmed as a key factor in tumour
development through the interactions of inflammatory mediators with gene expression, cell proliferation, and apoptosis.
Pancreatic cancer (PC) is one of the most aggressive and deadliest forms of gastrointestinal cancer. A large case-control
study found that aspirin, an anti-inflammatory drug, was associated with a decreased risk of PC. Moreover, aspirin has
been shown to have inhibitory effects on PC in both in vitro and in vivo studies. However, the clinical data analysis has
not been similarly promising. Results from genetic and pharmacological studies suggest that the anti-tumour effects of aspirin
are mediated, at least in part, through the inhibition of COXs. Furtermore, other results suggest that the chemopreventive
and therapeutic effects of aspirin are also mediated through COX-independent mechanisms. The COX-dependent
and COX-independent mechanisms will be described in this review. In addition, we will discuss future research directions
on the risks and benefits of the use of aspirin to treat PC and the potential cellular/molecular.
Keywords: Aspirin, anti-cancer therapy, chemopreventive effect, cellular target, COX2, inflammation, non-steroidal antiinflammatory
drugs, pancreatic cancer.
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