These results reveal that the JB oil acted as a chemopreventive dietary agent, inhibiting cell proliferation and COX-2 expression and inducing apoptosis, resulting in a significant reduction in colon tumor formation.
Moreover, CCL2 antagonists decreased intracolonic macrophage infiltration and COX-2 expression, attenuated neovascularization, and eventually reduced the numbers and size of colon tumors, even when given after multiple colon tumors have developed.
Collectively, our data indicate that COX-2 promotes colon tumor progression, but not initiation, and it does so, in part, by activating EGFR and Akt signaling pathways.
We examined the functions of HuR and TTP during colon tumorigenesis and their ability to regulate cyclooxygenase (COX-2), a mediator of prostaglandin synthesis that increases in the colon tumor microenvironment.
To further explore how cancer cells exploit the progrowth actions of prostaglandins while suppressing the proapoptotic actions of intracellular arachidonic acid, we determined the cytoplasmic phospholipase A(2) (cPLA(2)) and COX-2 expression levels in a panel of human colon tumors by immunohistochemistry.
Cyclooxygenase catalyses a key step in prostaglandin biosynthesis, and recent work suggests that one isoenzyme, COX-2, has important roles in early stages of pregnancy; it also appears to be involved in the somewhat analogous process of colon tumor formation and spread.