TGF-β1 mediates the effects of aspirin on colonic tumor cell proliferation and apoptosis.

Previous studies have demonstrated that aspirin serves an important role in chemoprevention and the suppression of colorectal cancer (CRC); however, the underlying mechanisms for this inhibition by aspirin remain unclear. Aspirin is capable of promoting apoptosis through prostaglandin-dependent orprostaglandin-independent signaling pathways. In the prostaglandin-dependent pathways, inhibition of cyclooxygenase (COX), particularly COX-2, is the primary mechanism known to be involved in aspirin-induced CRC suppression. Previous studies have implicated prostaglandin-independent signaling pathways and certain associated proteins, including SOX7, in aspirin-induced CRC suppression. In the present study, a newly-characterized association between aspirin, transforming growth factor (TGF)-β1 and CRC inhibition was identified. Specifically, aspirin triggers CRC cell apoptosis by inducing the secretion of TGF-β1, and the increased TGF-β1 then leads to apoptosis and proliferation inhibition in CRC cells.