Open AccessTGF‑β1 mediates the effects of aspirin on colonic tumor cell proliferation and apoptosis
Author(s) -
Yuyi Wang,
Chi Du,
Nan Zhang,
Mei Li,
Yanyang Liu,
Maoyuan Zhao,
Wang Feng,
Feng Luo
Publication year - 2018
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2018.8047
Subject(s) - aspirin , apoptosis , oncogene , cancer research , transforming growth factor , cell cycle , signal transduction , cyclooxygenase , cell growth , prostaglandin , prostaglandin e2 , biology , medicine , microbiology and biotechnology , endocrinology , biochemistry , enzyme
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.