Ibuprofen Inhibits Colitis-Induced Overexpression of Tumor-

摘要: The serrated pathway to colorectal tumor formation involves oncogenic mutations in the BRAF gene, which are sufficient for initiation of hyperplastic growth but not progression. A previous analysis tumors revealed that overexpression splice variant Rac1b occurs around 80% with mutant and both events proved cooperate cell survival. Here, we provide evidence increased expression patients inflamed human colonic mucosa as well following experimentally induced colitis mice. increase mouse model was specifically prevented by nonsteroidal anti-inflammatory drug ibuprofen, also inhibited cultured HT29 cells through a cyclooxygenase inhibition–independent mechanism. Accordingly, presence ibuprofen led reduction survival vitro Rac1b-dependent xenografts. Together, our results suggest stromal cues, namely, inflammation, can trigger changes colon identify highly specific efficient inhibitor tumors. Our data use may be beneficial treatment or inflammatory syndromes.